Handbook of Sports Medicine

Section 1 - Fundamentals1. Sport and medicine - the human raceEugene Sherry

2. Epidemiology of sporting injuriesEugene Sherry

3. Basic sports medicine scienceDiana E Thomas, Jane Gorman, John Rooney, and Simon Hutabarat

4. Medical problems of athletesEugene Sherry, Sameer Viswanathan, Amitabha Das, and Lawrence Trieu

Section 2 - Injuries

5. HeadLaurie Geffen, Anton D Hinton-Bayre, Saul Geffen, and Gina Geffen

6. Eye and faceLawrence Trieu

7. SpineJohn D Yeo

8. ShoulderEugene Sherry

9. ElbowEugene Sherry

10. Hand and wristEugene Sherry

11. Hip, thigh, and pelvisEugene Sherry

12. KneeEugene Sherry

13. Foot and ankleEugene Sherry

14. Gastrointestinal and genitourinaryJohn A Cartmill

Section 3 - Special Problems

15. Drugs and the athleteMark A Freeman

16. Nutrition for sportLouise M Burke

17. Dermatology and the athlete

Diana Rubel

18. Psychology and the athleteBarry Kirker

19. Rehabilitation of sports injuriesPhilippa Harvey-Sutton and Saul Geffen

Section 4 - Special Groups

20. The disabled athleteStephen F Wilson

21. The child athleteEugene Sherry

22. The old athleteSue Ogle, Greg Bennett ,and Tom Gwinn

23. The female athleteSameer Viswanathan and Jeni Saunders

Section 5 - Organization

24. Protective equipment in sportJohn Estell

25. Organization of sporting eventsManuel F Cusi

26. Diving medicineCarl Edmonds

Introduction When it happened Why it happened How it happened What will happen

Introduction

Sports medicine is concerned with the care and the potential performance of the athlete. It requires a comprehensive approach; unlike the fragmentation seen in technological medicine this century (today's medical students know more about T4 cell levels than a simple Colles' fracture). These principles of care were established by Herodicus of Selymbria (at time of Socrates) and Claudius Galen (131-201 AD) 1.. They emphasized training, diet, massage and a medical approach to athletics.

Galen's contribution to scientific medicine was monumental. He placed the clinical instructions of Hippocrates on a sound experimental basis; for 1500 years his works dominated medical knowledge. He was a true sports medicine practitioner (the father of sports medicine). Pontifex Maximus made him physician to the gladiators in the

Pergamon arena in Asia Minor (158-161 AD) and he published his methods of treatment (among his 500 known works). It is well to set Galen's contribution among others.

When it happened

A history of significant sports medicine events is outlined:

Event SignificanceBowling Game (Egypt, 5000 BC) Exercise with weights (Urina, 3600 BC) Chariot races (Greece, 1500 BC) Chinese book of Gung Fu (Circa 1000 BC)

Systematic teachings of exercise therapy

Text of the Hindu Atharva - Veda (Circa 1500 BC) Ancient Olympics (776 BC) Run of Pheidippedes (Marathon to Athens, 490 BC)

Heroism inspired Olympic ideals

Herodicus of Selymbria (time of Socrates 469-399 BC)

Emphasized medical gymnastics

Iccus of Tantrum (444 BC) First treatise on athletic trainingClaudius Galen (131-201 AD) 'Father of Sports Medicine'

Quintes of Sumerian (circa 4th century AD)

Described treatment of ankle sprains and boxing wounds

First rowing regatta (Venice 300 AD) Birth of the 'sacred' boat race (later cherished and idealized at Eton)

Avicenna (979-1037 AD) 'Father of Islamic Medicine' Relevant writings during post-crusade period

First cricket game (UK, 1250) Bergerius (1370 - 1440) Regular exercises for childrenGeronimo Mercuriali (1530- 1606) First illustrated book on sports medicineBenjamin Franklin (1706-90) Recommended resistance exercisesFirst Rugby Union game (Rugby School, 1823) Oxford-Cambridge Boat Race (1829) Edward Hitchcock MD (1854) America's first college team physicianJohn Morgan's paper on longevity of old oarsmen (mid 19th century)

Benefits of exercise scrutinized

Modern Olympic Games (1896) Greek doctors in attendance at marathonDeath of Lazaro, a Portuguese runner, from heat stroke after Stockholm marathon (1912)

Physical exams subsequently required for marathoners

Paris Olympic Games (1924) First US team doctor in attendanceInternational Federation of Sports

Medicine (FIMS) founded by Sr. Moritz (1928)

Berlin Olympic Games (1936) Nazi political perversion of Games

First Paraplegic Games (1948) Sport for all

First Asian Games (1951) Reflecting improved standards of nutrition and health

American College of Sports Medicine founded (1954)

4 minute mile by R.G. Bannister (1954)

'Physiological barrier' broken (3 min 59.4 sec), 'glimpse of the greatest freedom that a man can ever know'

President's Council (Eisenhower, 1956)

on youth and fitness US Governmental efforts to promote physical fitness through sport

American Academy of Orthopaedic Surgeons establish Committee on Sports Medicine (1962)

Formalization of orthopaedic surgeons' long-term involvement with care of athletes

Terrorism at Munich Games (1972) Terrorism at the GamesBlack Boycott, Montreal Games (1976)

Politics at the Games

Olympic competitors keep sponsorship money (1981)

End of amateurism

Ben Johnson, 100m sprint, banned for steroid use (1988)

'End' of use of drugs for performance enhancement

'Unified Team' at Barcelona (1992) 'End' of communist domination of Games

'Coca-Cola' Games in Atlanta (1996)'Beginning' of corporate control of sports (? started in LA 1984)

Today sports medicine has evolved into a respected discipline with dedicated associations, colleges, institutes and literature in most countries.

Chapter 2

Epidemiology of Sports Injuries

Introduction Investigating sports injuries Steps in study design and implementation Example: trends in skiing injuries in Australia Overview of sports injury rates

Introduction

Epidemiology is the medical discipline which deals with the occurrence, causes and prevention of disease. Its methodology, used in public health to study outbreaks of disease and to design preventive measures, is widely applied in sports medicine to injury rather than illness or disease. The epidemiological approach contributes much to better understanding of the incidence and causes of injuries and allows planning of prevention programs and the proper allocation of medical resources.

An understanding of the implications of assumptions inherent in the statistical methods underlying epidemiological methods is necessary if some common pitfalls are to be avoided (e.g. no clear hypothesis under test, poor definition of injury type, inappropriate controls, population under study not defined, over-generalization of results).

Snow skiing injuries have been extensively studied as has American football (because of the high incidence of head and spinal injuries). Interventional studies now being published examine the role of knee and ankle braces in injury prevention. With time more multi-centre studies will be planned to gather data on the effects of interventional measures.

Investigating sports injuries

Epidemiological approaches to sports injuries may be descriptive or analytical (1,2). Descriptive studies define the problem in terms of incidence and prevalence. Analytical studies seek to identify risk factors with the goal of doing something about the injury rate, or to evaluate the effectiveness of treatment regimes.

Incidence and prevalence

Incidence (rate) of injury is the number of cases per unit time. The rate of injury is measured as the number of injuries or injured athletes (note the significance of the distinction in relation to multiple injuries which may be of different type) over a specified period, and may be expressed in absolute or relative terms (e.g. 3.0 skiing injuries per 1000 skier days). The risk of injury (the probability that an individual will be injured) is measured in the exposed population as a cumulative incidence giving the proportion injured, by actuarial methods (difficult) or from incidence densities. These two parameters provide the basis for most studies of sports injuries.

Risk factors

Identification of risk factors provides a means for doing something about the sports injury problem. Both the observational and experimental approaches of analytical epidemiology are used (3).

Observational study designs are of three main types:

1. Case-control (Fig 1) - the injured group is compared with a non-injured group in relation to a potential risk factor. Such studies are retrospective, easy to conduct and commonly used, but careful matching of controls is important. The possible sources of bias, role of sampling vagaries and confounding variables must be carefully assessed.

2. Cohort (Fig. 2) - similar design, but prospective in that groups exposed or not exposed to a potential risk factor are recognized before injury and then followed through time. This approach is less susceptible to information bias (see below). data collection takes longer and the method is more expensive to implement . Variations include surveillance designs (continuous monitoring of a group of athletes as under the National Athlete Injury/Illness Reporting System in the USA or NEISS). In survival designs, survival curve analysis is used to follow the reduction in proportion of uninjured/injured over the study period (as in follow-up of orthopaedic joint replacement).

3. Cross-sectional (Fig. 3) - documents injuries and risk factors at one point in time, describing prevalence and injury patterns. This approach is of limited value where rehabilitation times after injury are long.

Experimental study designs are interventional. Subjects are assigned randomly to treatment or control groups (e.g. prophylactic wearing of ankle splints in basketball). Ethical problems may arise in relation to allocation/withholding of potentially useful treatment.

Effectiveness of treatment

The effectiveness of treatment is best studied in randomized clinical trials (Fig. 4) which should be double blinded as compliance with protocol is otherwise difficult to achieve. The study plan covers selection of patients (inclusion and exclusion criteria must be clearly defined), random allocation of treatments, treatment and analysis.

OXFORDHANDBOOKOF SPORTSMEDICINE

Section I Exercise and Metabolism

IntroductionCardiovascular response to exercisePulmonary response to exerciseQuantifying exercise capacitySkeletal musclesSystems for the provision of energy during exerciseFuel substrates for exerciseFuel regulation during exercise

Regulation of body temperatureTrainingFatigueExercise science

Section II The Framework of the Body

BoneJointsSkeletal muscleNervesTendonsLigaments

Introduction

Knowledge of the biochemistry and physiology of exercise is essential for interpreting the complex reactions involved in physical exertion. This knowledge can be applied to improve not only the performance of athletes, but also to monitor the health of the exercising public and to improve some medical conditions. Exercise has beneficial metabolic effects relevant to many areas of medicine, such as in diabetes, in the prevention of atherosclerosis and obesity, and in the management of stress. Regular exercise lowers: the resting heart rate, blood pressure, diabetic insulin requirements, LDL (low density lipoprotein) and triglycerides, while it increases: HDL (high density lipoprotein) and lean body mass. With appropriate exercise, the cardiovascular capacity overall improves and the cardiovascular risk is lowered. In some medical conditions fatigue occurs after mild exertion e.g. peripheral vascular disease. From information based on the metabolism of exercise and the ensuring fatigue, assessment and treatment can be implemented through strategies such as suitable nutrition and training programs.

In general genetic reproduction, adaptive capability, and metabolism maintain the human condition. You walk (if intelligent, rather than run) to do kill your prey in the jungle or boardroom with sword or pen, carry it home and then write a letter to your mother (historical record = civilization) about it. There are 65 billion body cells, about 50% are muscle cells which require the delivery of nutrients and the removal of waste products (increased demand with exercise). This is met by the cardiovascular

and pulmonary systems.

Cardiovascular response to exercise

During exercise, the cardiac output increases, enabling the cardiovascular system to increase the transport of oxygen to the working muscles and to remove the metabolic heat produced by transferring it to the skin surface for evaporation, while still maintaining the blood pressure to supply blood to the brain. Maximum exercise capacity is determined by increased O2 delivery from increased cardiac stroke volume and so cardiac output (CO = SV x HR), vasodilatation and to a much lesser extent increased mitochondrial volume. Such capacity decreased with age from reduced max HR and reduced SV, although exercise may maintain it. See Athlete's Heart discussed in Chapter 4.

Pulmonary response to exercise

During exercise, the pulmonary ventilation also increases in order to augment oxygen supplies to the exercising muscles and remove waste carbon dioxide from the increased oxidative metabolism. Exercise improves the efficiency of the respiratory muscles and increases the total lung capacity by reducing the residual volume. The vital capacity is increased and elite athletes have very large vital capacity. The maximum minute volume is also increased by athletic training and endurance athletes are able to process large volumes of air during competition (from 6L/min at rest up to 120L/min during exercise) (Newsholme and Leech 1994). In fact, the athletes pulmonary capacity may determine full metabolic potential and who becomes a champion (i.e. those with the largest 'vital capacities').


Section I The Environment and Sport

IntroductionHeatWet bulb globe temperature (WBGT)Heat problems

Cold problemsAltitude problems

Section II Acute management of the sick and injured athlete

IntroductionSick and injured athletesCare of the collapsed or seriously ill athleteCommencing of early CPRThe seriously injured athleteExercise testing and prescription

Section III Medical Problems in Sport

Diabetes mellitusRespiratory problemsGastrointestinal problemsCardiac conditionsHeadacheFatigueChronic fatigue syndromePseudonephritisExercise and the immune systemEpilepsyConclusions

Introduction

Athletes do battle with themselves, their competitors and the environment. The result maybe glory, injury or illness. In this chapter we describe the medical and environmental problems facing athletes. Many are potentially serious but often maybe prevented by proper preparation and education.

Heat

It is important to understand thermoregulatory factors. Thermoregulation results from reflex responses from the various temperature receptors in the skin, central vessels, viscera, and (preoptic area) anterior hypothalamus, signalling sympathetic shunting of blood and sweat gland stimulation when temp>37°C (Benzinger reflex). It is well depicted in Fig 1. The body maintains core temperature between the normal range of 36.1 to 37.8°C by balancing heat production/gain and heat loss. Heat is produced by metabolic functions (65 to 85 kcal/hour at rest) and work done by muscles (both smooth and

skeletal; muscular contraction produces 300to 700 kcal/hour). Heat is gained by radiant energy from the sun(100 to 200 kcal/hour).Fever can add at a rate of 15% rise per degree F of fever. Heat is lost to the environment in the following ways:

· Radiation (65% heat loss, only works when body temp>ambient temp) · Evaporation (sweating, air-skin interface, the latent heat of evaporation is the amount of heat passed to the environment by vaporization (0.6 kcal of heat/ml sweat), it is the major physiological defense against over heating as the ambient temperature rises, reduced by high humidity as the ambient vapour pressure approximates moist skin). · Convection (needs air movement,12 to 15%) · Conduction (direct contact) · Reflected Radiation (from nearby surfaces)

Wet Bulb Globe Temperature (WBGT)

It is important to evaluate all aspects of the exercise environment viz. temperature, humidity, air movement (if outdoors) and solar radiation. This is done by the Wet Bulb Globe Temperature (WBGT) which is a single temperature, which is dependent upon air temperature, solar & ground radiation, humidity and wind velocity. It thus represents a sum of the impact of the environment upon the athlete. It can be measured with cheap simple instrumentation or calculated with data from the weather bureau (either degrees F or C).The WBGT calculation uses three measurements-natural wet-bulb temp(place a wetted wick over the thermometer bulb), air temp, and globe temp (temp. inside a copper globe painted flat black). It is calculated thus: · Indoor WBGT = (0.7 x natural wet-bulb temp) + (0.3 x globe temp) · Outdoor WBGT=(0.7 x natural wet-bulb temp) + (0.2 x globe temp) + ( 0.1 x air temp)

Whether to or how to exercise in hot environments can be decided by considering the two criteria-RAL (Recommended Alert Limit - above which action should be taken to reduce heat stress) and - C (Ceiling Limit, above which exercise should not be undertaken without somehow changing the environment). This is illustrated in Fig 2.. This graph presents limits based on exercise intensity (energy expenditure per hour) and WBGT. When the temperature is between C and RAL exercise is OK but with risk; therefore suggest this: ·

Change the environment (fans or air conditioning) or move to area where WBGT is within acceptable limits ·

For the exercise session, decrease the intensity of the exercise (slow the pace and/or add rest periods).Useful guide is the TARGET HEART RATE (unchanged from cool conditions) .Exercise HR is increased one beat/min for every degree Centigrade above 25°C and two beats/min for every mmHG above 20mmHg water vapour pressure. Stick to a determined HR.

Marron and Tucker have provided a useful guide for exercise in the heat: Table 1

It is important to acclimatize to exercise in a hot environment.25% of the thought-to-be healthy population maybe heat intolerant if unacclimatized (but will decrease to 2% with proper preparation with aerobic exercise starting with a 10-15 min and over a 10-14 day period). Especially for those > 60 years (as thirst becomes less useful guide to hydration). The following conditions predispose to heat stress:

· HBP (alters control of skin blood flow)· diabetes (because of neuropathy) · drugs (diuretics, *-blockers, *-agonists, vasodilators, opiates, salicylates, thyroxine, CNS stimulants, parasympatholytic or anticholinergics) · alcohol · obesity · prior heat tolerance problems

The American College of Sports Medicine in 1984 recommended that endurance events were unsafe to be held if the WBGT >28 degrees celcuis.

highest in combat sports, such as boxing, where the head is a legitimate target. However, head injury is also common in contact sports such as the various codes of football, especially gridiron, where the annual incidence may be as high as 10 - 20% of participants, and rugby, which has up to twice the risk of other (non gridiron) football codes (2, 3). Other non-contact sports with a higher risk of head injury include motor racing, equestrian and gymnastic events, snow, board and blade sports, and cycling. Sports where head injury is rare but potentially severe include golf, shooting, cricket, baseball, and field hockey.

The focus in this chapter is on brain injury. However, head injuries often involve significant damage to scalp, skull, meninges and blood vessels as well as the face, jaws, eyes, ears and neck. While the initial assessment and management of head injury described in this chapter includes injuries to these other tissues and sites, the subsequent management of extra-cranial head injuries is dealt with in Chapters 6 and 7.

The most common form of head injury in sport is an episode of concussion (Latin: concutere, to shake violently), from which a full recovery is usual. However, any head injury can have immediate or delayed life threatening consequences and serious long-term sequelae. As such, all head injuries require thorough systematic assessment by the sports physician (a) to recognise and manage the acute consequences, including the prevention of secondary brain damage (b) to arrange the safe transfer of the injured athlete to an appropriate treatment facility when necessary or (c) to ensure that the athlete is closely monitored for at least 24 hours and returns to participation only when fully recovered. Finally, (d) prevention also needs to be addressed by the sports physician. · This chapter has five main sections:

Mechanisms of brain injury, which provides a summary of the anatomical, physiological, and pathological issues that influence management and prevention.

Clinical features of brain injury, including symptoms and signs of concussion. On site assessment and management of head injuries. Post acute assessment and management of concussion, which includes clinical and psychometric

assessment of recovery and guidelines for the return to participation in sport. Prevention measures including athlete preparation, protective devices and rule modifications.

Mechanisms of brain injury

Head injuries in sport usually result from direct impact of the head but can occur when the head is subjected to forces translated from elsewhere on the body. Brain injury may be primary, due to the direct application of physical forces damaging brain and associated vascular tissue, or secondary, arising from intracranial and extracranial complications of injuries to the head and other parts of the body (4, 5, 6).

Forces producing brain injury

Forces acting on the brain produce three types of tissue stress: compressive, tensile, and shearing. Compressor forces tend to produce focal contusions and if relieved promptly produce the least long-term consequences. Tensile (stretching) forces act mainly on long fibre pathways and damage tends to be more diffuse (diffuse axonal injury). Shearing forces operate parallel to surfaces and can produce serious consequences by tearing brain and vascular tissue. · Most forces are dynamic and result in propulsion and rotation of the brain within the cranium following impacts to either the head or body. Cerebro spinal fluid (CSF) dissipates focally applied forces and permits gliding of the hemispheres within the cranium.

A forceful blow to the head usually produces maximal brain injury at the site of impact (coup injury) particularly if the head is stationary before impact. A moving head striking a non-moveable surface, as in falls or collisions, may also produce brain injury at the opposite pole of the cranium (contra coup injury). This is because the brain lags behind in the moving cranium, thereby squeezing protective CSF away from the trailing pole (Fig 1).

The magnitude of any force is the product of mass and acceleration (Newton's Law). If the neck muscles are tensed at impact, the mass of the head approximates that of the whole body and acceleration (or deceleration) of the head is greatly reduced for any given force. Conversely, when the head is not braced, as in unanticipated blows or further blows in an already stunned state, a given force produces much greater acceleration of the head.

Pathophysiology of primary brain injury

Gliding of the brain within the cranium is impeded at three main sites (a) dura mater - brain attachments e.g. midline falx cerebri and tentorium cerebelli (b) irregular and protuberant surfaces of the frontal and middle fossa of the base of the skull (c) wherever CSF is dissipated by acceleration, especially at the poles of the frontal and temporal lobes.

Focal contusions occur mainly at or opposite sites of impact and comprise local petechial haemorrhages and necrotic damage, which are often accompanied by surrounding oedema and subarachnoid haemorrhage.

Propulsion and rotation of the hemispheres on the relatively fixed brainstem may cause damage to ascending brain stem pathways, ranging from stretching with transient impairment of consciousness to tearing of subcortical fibre tracts with immediate unconsciousness and coma.

General cerebral oedema due to a combination of local metabolic derangement, breakdown of the blood-brain barrier and obstructions to venous outflow, leads to a rise in intracranial pressure (see below).

Pathophysiology of secondary brain injury

Head injuries may result in complications that are life threatening and can have serious long-term consequences. Because they are often remediable in their early stages, they require immediate attention.

Intracranial complications

Intracranial complications include skull fracture, intracranial haemorrhage, raised intracranial pressure, cerebral hypoxia, and infection.

Skull fractures may result in direct brain compression, intracranial bleeding, CSF leaks and infection. Brain injury may occur without a skull fracture; however the presence of a skull fracture greatly increases the risk of intracranial bleeding and infection. The site of a fracture is also critical in anticipating complications e.g., temporo-parietal damage to meningeal vessels, frontal damage to sinuses. Fractures may be either of the vault or the base of the skull.

- Vault fractures, which may be linear or depressed, are usually associated with scalp haematomas or a localised area of swelling and tenderness.

- Basal fractures are harder to detect and usually involve intracranial bleeding. Periorbital haematomas, subconjunctival haemorrhage and CSF rhinorrhoea are signs of an anterior fossa fracture; CSF otorrhoea, haemotympanum and retromastoid bruising (Battle's sign) are signs of a petrous bone fracture.

- Close observation and radiological investigation are required for all suspected skull fractures. Opinions differ on the value of routine CT scan for all mild head injuries. Early CT scan and early discharge of patients with normal radiological and neurological findings has been advocated as being as safe and more cost effective than hospitalization for observation with CT scan performed only after clinical deterioration (7).

- Intracranial haemorrhage may result in local compression, raised intracranial pressure, and ischaemia to the area of supply of the damaged vessel. All intracranial haematomas constitute a priority in the management of head injury because of their immediate threat to life and eventual recovery of function and because they may be surgically remediable. Haematomas may develop immediately or some time after the initial injury preceded by a lucid interval. Delay in recognising and treating intracranial bleeding is the most common cause of avoidable mortality and morbidity due to head injury. Vigilance needs to be maintained for at least 24 hours. The four types of intracranial haemorrhage are:

(a) Extradural haematomas result from shearing forces or skull fractures that tear blood vessels supplying the dura and skull. Haematomas may form rapidly (high pressure bleeding between dura and skull) and compress the brain leading to early

loss of consciousness and localising neurological signs or they may occur up to several hours following the initial injury.

(b) Subdural haematomas are the most common form of sports related intracranial bleeding. Shearing and direct impact forces tear small veins resulting in low pressure bleeding between the brain and dura matter. Signs and symptoms may be subtle and develop insidiously over days or even weeks.

(c) Subarachnoid haemorrhage may result from any head injury, however mild. Severe headache and localising signs usually develop rapidly.

(d) Intracerebral haemorrhage occurs with major brain injury. Intraventricular haemorrhage may lead to subsequent blockade of CSF outflow. Brainstem haematomas are life threatening.

Raised intracranial pressure is a serious consequence of brain injury that may result from several causes including depressed fractures, hypoxia, hypercapnia, hyperperfusion, hypoperfusion, intracranial haemorrhage, and intracranial infection. Raised intracranial pressure leads to cerebral compression, which may be followed by herniation around the brainstem with venous obstruction and infarction. Signs include fluctuations in consciousness, fits and focal neurological deficits.

Two rare conditions are associated with life threatening rises in intracranial pressure after even minor head injuries

- Malignant brain oedema syndrome occurs in children and adolescents as diffuse brain swelling with extreme hyperaemia. It may be due to loss of autoregulation but the mechanism is unknown. After even relatively minor head injury, there is a deterioration of consciousness resembling, in its rapidity, extradural bleeds in adults. Prompt intubation and measures to reduce intracranial pressure such as hyperventilation and osmotic diuretics are required. The mortality rate is high.

- Second impact syndrome is a variant of malignant brain oedema syndrome that is seen in adults following even minor head trauma when still suffering symptoms of a previous head injury. Loss of autoregulation precipitated by an unknown mechanism leads to massive and diffuse hyperaemia and oedema of the brain. Intracranial pressure rises within minutes and may lead to herniation and coma. Prompt measures to maintain respiration and reduce intracranial pressure as above are indicated. The mortality rate approaches 50% and morbidity is near to 100%.

Hypoxia due to loss of CNS control of airway patency and breathing may occur following either serious primary injury to the brain stem or may be secondary to raised intracranial pressure with brain herniation. Brain hypoxia may also result from extracranial complications (see below).

Infection (meningitis or brain abscess) may occur when the dura is penetrated. Direct contamination of the intracranial cavity may occur in compound depressed fractures of the vault, whereas contact with middle ear cavity and nasal sinuses may introduce infection in basal fractures.

Concussive convulsions seen within seconds of insult are to be distinguished from later epileptic seizures. Such concussive convulsions are rare, transient and do not necessarily lead to the development of epilepsy (8).

Post-traumatic epilepsy may develop within days to months. It usually follows traumatic brain injury with prolonged periods of unconsciousness, and occurs in about 23% of hospital admissions of sports-related head injury (9). C Extracranial complications

Extracranial complicationsof head or associated injuries may interfere with brain metabolism and perfusion. Given

the immediate dependency of brain tissue on its oxygen supply and the potential for remediation of many of the complications, recognition and management of extracranial causes of secondary brain damage constitutes a clinical priority. Causes include injuries interfering with ventilation, such as chest, neck or facial injuries that obstruct airways and affect chest movement, and injuries interfering with brain circulation by producing haemodynamic instability and hypovolaemia.

Non-traumatic sports related brain injury

There are two main causes of non-traumatic sports related brain injury (10).

Cerebral air embolismunique to underwater diving, second most common cause of death after drowning · occurs in rapid ascents from > 10 metres· symptoms may occur within moments to hours of surfacing · signs include: seizure, hemiplegia, diplopia, tunnel vision, vertigo, or dysarthria · if diver surfaces unconscious, diagnosis is strong presumption · seek to recompress subject as soon as possible

High-altitude cerebral oedema accounts for up to 5% of deaths above 4000 metres · symptoms develop within 72 hours and include ataxia, vertigo, confusion, and hallucinations · immediate treatment is return to lower elevation and oxygenate · monitor for signs of raised intracranial pressure and treat accordingly

side) and occasionally paraesthesia in the ulnar nerve distribution. Valgus deformity and elbow contracture may follow. Valgus stress testing with the elbow at 30 degrees of flexion displays increased laxity and pain. Incongruity develops between the olecranon process and its fossa with loose body formation at the medial side of the olecranon. X-ray's may show osseous bodies in the MCL or fluffy calcification at the tip of the olecranon.Treatment is rest, activity modification, NSAIDs and physiotherapy. If posteromedial pain continues then arthroscopy is necessary to debride the osteophytes. If there is chronic MCL laxity or instability then surgical reconstruction (primary repair or use palmaris longus is necessary.Acute rupture of the MCL

Isolated tears of the anterior oblique ligament may occur in javelin throwers. The mechanism is almost pure valgus stress with the elbow flexed at 60-90 degrees. There is severe pain and a pop on the medial side of the elbow. Ulnar nerve symptoms may occur with ecchymosis about the elbow (48 hours later). If the diagnosis is in doubt stress tests or stress x-rays are useful . Acute repair of the ligament is necessary.Valgus extension overload

Seen in pitchers during the acceleration phase. (In the early phase of acceleration excessive valgus stress is applied to the elbow causing impingement). There results osteophyte formation posteriorly and posteromedially which can cause chondromalacia with loose body formation.

The pitcher presents with pain on pitching (early in the game) and are not able to let go of the ball. Pain over the olecranon fossa occurs in valgus and extension. X-rays show a posterior osteophyte at the tip of the olecranon (on lateral views).Treatment (should be started early) is increasing functional strength, heat and ultrasound. An osteophyte needs surgical excision).

Posterolateral rotatory instability(1)Differentiate from a frank elbow dislocation. Caused by a laxity or disruption of the ulnar part of the lateral collateral ligament which then allows a transient rotatory subluxation of the ulno-humeral joint (and secondary dislocation of the radio-humeral joint).

There maybe preceding trauma (dislocation or sprain from a fall on an outstretched hand). Previous surgery, radial head excision or lateral release for a tennis elbow, maybe the cause of instability.

There is a history of a recurring click, snap, clunking, locking of the elbow and a sense of instability that ones elbow is about to dislocate. Such stability episodes occur with a loaded extended elbow and supinated forearm. Examination, often unremarkable, should include the 'Lateral Pivot Shift' (Posterolateral rotatory apprehension test)(Fig 2- Performed with patient supine, preferably under general anaesthesia; The elbow is extended overhead and the forearm fully supinated; A valgus and supination force is then slowly applied to the elbow going from the extended to flexed position; This results in subluxation of the ulno-humeral joint and radio-humeral joint ).

On X-ray the joint will look normal (unless taken with the joint subluxed) so the diagnosis is made from history and after above test. When symptomatic surgery is required (re-attach the avulsed lateral ulnar collateral ligament or reconstructing it (with a tendon graft).

Tennis elbow (lateral epicondylitis)

A lateral tendinitis which involves the origin of Extensor Carpi Radialis Brevis. It is related to activities that increase tension and stress on the wrist extensors and supinator muscles (not all activities include tennis. It occurs between the ages of 35-55 years with pain localized to the lateral epicondyle especially after a period of unaccustomed activity (such as tennis 3-4 times a week). The pain is worsened by movements such as turning a door handle or shaking hands. Examination reveals pain localized to the lateral epicondyle and distally. Typically aggravated by passive stretching the wrist extensors or actively extending the wrist with the elbow straight (Fig.3 ).X-rays are often normal (to exclude OA, LB or tumour). A bone scan will show increased uptake about the lateral epicondyle. An ultrasound or MRI will show degeneration within the belly of ECRB. The differential diagnosis includes: posterior interosseus nerve entrapment ( has a more distal localization of the pain and associated weakness); radial tunnel syndrome (pain distal and exacerbated by resisted extension of long digit, i.e. ECRB); OA/LB/Tumour.It will resolve over a 10-12 month period but there is a 30% recurrence therefore treat comprehensively(1) with rest, activity modification, NSAIDs, heat, ultrasound, phonophoresis with 10% hydrocortisone cream, brace (counterforce effect), eccentric muscle strengthening, modify tennis handle (usually too large) or tennis stroke (occurs in back hand stroke). injection of cortico-steroid (no more than 3, just below ECRB, anterior and distal to the epicondyle), and then surgery (symptoms >12 months, release and excise ECRB, note Nirschl scratch effect). Return to sport when strength 80% back or after 4 to 6 months.1 S W O'Driscoll, D F Bell, B F Morrey 1991. Posterolateral rotatory instability of the elbow JBJS 73A 440


Biomechanics

Damage to the spinal vertebral column

Assessing the problem

Clinical analysis of sensory and motor disturbance

Soft tissue injury

Prevention

Biomechanics

Anatomy of the spinal cord

Within the human spinal canal the spinal cord extends from the base of the brain to the conus medallaris usually at the level of the L1/L2 vertebrae when the nerve roots become the cauda equina. The spinal cord is a soft, pliable mass of nerve fibres and cells supported by glial tissue and enmeshed in small blood vessels. The cord contains myelinated 'long' tracts and interconnecting fibres described as the 'white matter' surrounding the central 'grey matter' comprising mostly unmyelinated nerve fibres with supporting glial tissue and a very intense small blood vessel network. Blood flow to the spinal cord is mainly provided to the anterior tow-thirds of the cord by the anterior spinal artery which arises from two branches of each vertebral artery over the medulla and runs superficially in the anterior sulcus to eventually synapse around the lower end of the spinal cord with the descending branches of the posterior spinal arteries which arise from the posterior inferior cerebellar arteries. Posterior spinal arteries provide blood flow to the posterior third of the spinal cord.

These small spinal arteries require additional assistance from the major supplementary arterial supply usually at two levels of the spinal cord (T1 and T11), from the corresponding intercostal arteries.

Nerve fibres in the posterior columns of white matter are essentially travelling cephalward and are uncrossed until higher in the central nervous system carrying sensory modalities for proprioception, vibration, some touch and appreciation of moderate degrees of temperature variation. Tracts in the anterior column of white matter are mainly travelling caudalward to synapse either directly with anterior horn cells or with other interneuronal pathways. In the lateral column there is a mix of fibres going 'upwards and downwards'. The lateral column contains the lateral cortico-spinal pathway (pyramidal pathway) for control of motor power and anteriorly is the main tract for pain (spino-thalamic) which are mostly crossed fibres. In the cervical spinal cord the nerves in this tract have a laminated arrangement with the most distant fibres travelling

towards the distal end of the body (sacral) and the cervical travelling more central within the tract. Anteriorly to the pain pathway is the main pathway for temperature and further anteriorly again is the pathway for touch. Touch appears to be transmitted in the anterior and posterior columns. The cortico-spinal pathway also has a layered orientation with those motor fibres destined to synapse with anterior horn cells in the lower spinal cord (lumbo-sacral) travelling in the more superficial layers of the tract in the cervical region. There remains a complex arborisation of synapsing fibres within the spinal cord and many interneuronal pathways are necessary to achieve balanced efferent and afferent activities within the human spinal cord. The spinal cord tends to occupy only 50% of the ligamentum denticulatum and in the intervertebral foramina.

The dura mater is also attached firmly to the base of the skull and at the second fused segment of the sacrum in the adult (filum terminale).

There is therefore a lateral attachment of the spinal cord to both sides of the spinal canal. The spinal cord within the dura is a mobile organ which tends to be held more tightly in the flexed position of the spine and in a more relaxed position when the spine is extended.

The spinal canal is formed by 26 vertebra, 24 usually being separate from each other but attached with intervening discs, ligaments and muscles. The coccyx is attached to the lower end of the sacrum and usually comprises 4 small fused vertebrae of a vestigial 'tail'. The sacrum usually consists of 5 vertebra also fused together. The stable spinal column is maintained with a cervical lordotic curve, a thoracic kyphotic curve and a lumbar lordotic curve. There are fixed kyphotic curves in the fused sacrum and coccyx.

The spinal vertebral column (Fig. 1) can be subdivided into the Denis 3 column classification, with an anterior column, which includes the anterior longitudinal spinal ligament, the anterior annulus of the disc and the anterior third of the vertebral body; the middle column under this classification includes the posterior spinal longitudinal ligament, the posterior annulus of the disc and the posterior two thirds of the vertebral body; the posterior column involves the posterior bony arch with the spines, laminae and pedicles, and attached ligaments including supraspinous, interpinous, ligamentum flavum and capsules of the posterior facet joints.

The muscles immediately surrounding the spinal column and attached to the vertebrae are of great importance in maintaining stability of the spinal column. In addition to those muscles which are closely applied to the vertebrae, there is the additional 'wider circle' of muscles which includes the larger spinal muscles, for example, trapezius, latissimus dorsi and the abdominal muscles.

Each disc has a firm annulus fibrosus surrounding the nucleus pulposus, which is softer, pliable material and each disc is firmly attached to the adjacent surfaces of the vertebra above and below. The posterior spinal longitudinal ligament is loosely attached to the discs. The annulus fibrosus has a nerve supply from the sinu vertebral nerve of Luschka.

Injury

Damage to the spinal cord can either occur from direct injury to the spinal cord tissue, including nerves, cells and supporting tissue (glia) within the spinal membranes or through injury to the blood vessels essential for cord function. Damage can occur to the anterior spinal artery, posterior spinal arteries and the circumferential arteries which give off radiate branches running into the deeper central regions of the spinal cord. There is also a complex network of very small vessels, particularly within the grey matter which can be injured. There is now evidence to suggest further progressive damage will occur to nerves in the spinal cord within hours of the initial injury due to changes which occur in microvascular tissue within both grey and white matter. The exact nature of these progressive pathological changes has yet to be fully identified. A lack of efficient blood flow to the partly damaged nerve tissue can lead to additional ischaemia and further damage to nerves which may have otherwise survived the initial direct injury.

Damage to the spinal cord is described as 'complete' if laceration or severe bruising has occurred at the level of the lesion. In adults this injury is frequently associated with disturbance of the bony canal following fracture or fracture dislocation. In children there is often no obvious radiological evidence of significant damage to the vertebral column. Less serious injuries are described as 'incomplete' spinal cord injuries, eg. in concussion where the pathological changes are reversible with scattered small areas of haemorrhage in grey and white matter without disruption of the cord structure.

Contusion, or bruising, which can be described as being (I)

'mild' where haemorrhages are larger in number and size than in concussion and with some permanent damage to nerve fibres and cells; (II) 'moderate' with increased damage and severe bruising resulting in complete loss of cord function.

The various areas of the spinal cord can be damaged resulting in specific clinical syndromes; eg. the Brown-Sequard syndrome where damage is confined mostly to one half of the spinal cord; the anterior column syndrome where the antero-lateral columns are affected often by damage to the anterior spinal artery; the central cord syndrome where the grey matter is the essentially affected area resulting in central cystic changes an profound loss of anterior columns without significant loss in other areas and this injury produces severe disability with loss of proprioception even though there is usually significant voluntary movement below the level of the lesion.

Damage to the spinal vertebral column

Bones

Fractures in the vertebral bodies are described as wedge fractures, from flexion and compression injuries; extension fractures are associated with 'shearing' translational injuries; compression fractures is a burst injury to the vertebral body with retropulsion; a slice injury which can occur as a flexion and rotation causing damage to the vertebral body and interspinous and supraspinous ligament between the vertebrae.

Spondylolysis (Fig. 2) occurs with a defect in the pars interarticularis of the vertebral body. If the defect is bilateral possible shift may occur in the anterior and middle column segments of the spine following separation from the posterior spinal column segment. This is described as spondylolisthesis (Fig. 3) and identified as grade 1, i.e. 25% of the shift forward of one vertebra in relationship to another, up to greater than 50% of the vertebral displacement (grade 4). Ligaments and joint capsules are usually damaged including the interspinous ligaments, facet joint capsules, posterior longitudinal and anterior longitudinal ligament to allow subluxation of facet joints with the anterior vertebral subluxation. These injuries can be found in fast bowlers, baseball pitchers, gymnasts and weight lifters.

Damage can occur to the intervertebral discs (Fig. 4) resulting

in mild bulging of the annulus, increasing to bulging with tearing of the fibrous annular tissue if more severe. Rupturing of the disc results when the nucleus pulposus herniates through a break in the annular wall frequently impinging on nearby spinal cord, cauda equina or emerging nerve roots.

Damage to specific vertebrae

The C1 and C2 vertebrae (atlas and axis) damage. Fracture of the C1 ring secondary to axial compression can result in a Jefferson type fracture. Rupture of the transverse ligament of the atlas produces instability. Consider potential instability if the atlanto-axial space is greater than 3mms in flexion in the adult and 4mms in a child. Fractures of the odontoid frequently produce pain which radiates posteriorly into the occipital area. The odontoid fractures are divided into type 1 where there is a small segment of the odontoid fractured; type 2 where the base of the odontoid is fractured; and type 3 where the fracture extends from the base of the odontoid into the body of the C2 vertebra.A 'hangman's fracture' (traumatic spondylolisthesis) occurs through the pedicles of C2 following hyperextension of the head and neck.

Damage to muscles, ligaments and tendons

Mild damage to muscles involves over stretch or direct bruising with more severe injury when muscle fibres are torn or disrupted at the insertion of the tendon. The ruptured fibres in the muscle belly will retract and ultimately heal with less elastic scar tissue.

The post traumatic inflammatory process can localise at the insertion of muscles, tendons and ligaments near bone and is described as enthesopathic inflammatory process which can lead to calcification. The sites commonly involved are the insertion of the outer layer of the annulus fibrosus into the vertebral body, sometimes causing bony bridges between adjacent vertebrae (syndesmophytes). Injury to musculo-skeletal tissue may highlight previously undiagnosed spondylarthropathies including ankylosing spondylitis, spondylitis associated with psoriasis, enteropathic syndromes, Reiter's disease and arthritis associated with positive 'rheumatoid factor'

OXFORDHANDBOOKOF SPORTS

MEDICINE

'It is his feet which confer upon man his only real distinction and provide his only valid claim to human status' - WF Jones, Mens place among mammals.

Biomechanics Assessing function Ankle and foot sprains Peroneal tendon injuryPosterior tibial tendon injuryAnterior tibial tendon injuryAchilles fendon injuriesGastrocenemius injurySpring ligament sprainCuboid syndromeSinus tarsi syndromeFractures Mid foot Stress fracturesNerve entrapmentCompartment syndromePlantar fasciitisOs trigonumTurf toeSand toeTibiotalar spursMetatarsalgiaFreiberg's infractionHallux valgusHallux rigidusSesamoiditisShort leg syndromePersistent painful ankle

Biomechanics

The foot has evolved from an arboreal grasping organ to an agent for motion, (probably over last 1.8 million years). The big toe became aligned with the shortened smaller toes, the subtalar joint became stiffer, the medial arch and a higher heel developed. The body is now supported on the sustentaculum tali with the calcaneus bowed under the ankle joint (Fig. 1). It is easily toppled from this ledge where it is balanced in tension by the lateral ligament complex.

Little wonder twenty five percent of all sporting injuries involve the ankle and foot. There are 23,000 new ankle sprains in the USA everyday (5,000 per day in the U.K.)

The tibio-talar articulation allows 25° dorsiflexion, 35° plantar flexion and 5° rotation. The instant centre of motion lies on a line along the tips of the malleoli and postero-laterally on the talar dome. Up to 5 times the body weight is transmitted across this joint.

Gait has two phases (Fig. 2 ): stance (60% of cycle; foot flat, heel off, toe off) and swing (40% of cycle; toe off/toe clear/heel strike). During walking one foot is always on the ground. In running both feet are off the ground at one point in the stride. The weight is borne from the heel, along the lateral border of the sole then inward across the metatarsal heads from the fifth to the 1st MTP joint. Stability is gained by the talar mortise and ligament support. The subtalar joint functions like a hinge and allows eversion and inversion. The mid-foot permits abduction and adduction. The forefoot provides flexion and extension. Pronation of the foot (5°) involves coupled dorsi flexion, eversion and abduction (sole turned down). Supination (up to 20°) involves coupled plantar flexion, inversion and adduction (sole turned up). The foot transmits 3 times the body weight during running, through 3 arches (medial, lateral, transverse). The second metatarsal is the keystone of the mid-foot in gait; the first metatarsal in the stance phase.

Biomechanical advantage in certain sports may result from Pigeon toes (sprinters, tennis, squash; sway-back (increased lumbar lordosis with anterior pelvic tilt) - sprinters, jumpers, gymnasts; duck (everted) feet- breastroke; inverted feet- backstroke, butterfly; double jointedness (ligamentous laxity)- gymnasts.

Susceptibility to injury is increased by: postural defects, muscle weakness/imbalance, lack of flexibility, malalignment problems (pronated feet, LLD with pelvic tilt); Training techniques (> 64Km/week of jogging) playing environment and equipment contribute. Pay particular attention t the athlete's footwear and ankle support. 'Sexy shoes painful feet the women's shoe wear problem'1- most of the forefoot problems of women can be traced to undersized, though sexy, fashionable shoes. Make an outline of the patients bare foot standing on a sheet of paper and note that it is often 2 to 3 shoe sizes wider than the sole of their shoe.

Sports specific injuries often associated with particular sports include: skiing- Peroneal tendon subluxation, nerve entrapment, plantar fasciitis; running- lateral ligament sprains, stress fractures, shin splints; ballet- os trigonum/FHL impingement, sesamoiditis, stress fracture, hallux valgus; football- turf toe, ankle and mid-foot fractures; tennis- gastrocnemius strains, TA injury, stress fractures; soccer- ankle sprains, stress fractures; basketball- lateral ligament sprains, plantar fasciitis, Jones' fracture; (diaphyseal fracture base 5th metatarsal) gymnastics- Severs' disease. (traction apophysitis of the calcaneus)

Assessing function

Gait Video analysis of gait on the track or field provides documentation and allows correction of incorrect posture in many sports. Footwear Examine wear patterns on shoes (excessive wear of the outer heel with tibialis posterior problems, blown-out medial shoe with hallux valgus) and /or check the wet footprint. Normal bearing points are centrally under the ball of the foot and postero-laterally at the heel. Note: Orthotics are more effective for planovalgus foot rather than pes cavus.

History Collect details of the mechanism of injury (high versus low velocity, spontaneous onset, rolled over on heel), problems shoe wear and athletic performance. Where is the pain localized, and other characteristics, is there stiffness of the ankle/subtalar joint(tarsal coalition) or big toe. Any swelling or instability (of ankle joint). Medical history. Previous injury.

Examine the whole patient (exclude other injuries and underlying medical condition e.g. diabetics, cerebral palsy) and the whole limb (alignment, flexion contractive hip, varus/valgus/flexion contracture knee). Review gait (limp present? antalgic/short-legged/neurological) and whether walk with foot extremely rotated (to avoid pain of roll through). Correlate with examination findings. Test power (heel stand, toe stand, stand on inside/outside foot) Assess medial arch (pes cavus or flat foot). Patient sits on bench, you sit at patient's foot with small stool between. Note extent and area of swelling. Carefully palpate: ankle joint (note point tenderness) from tip medial malleolus to tip lateral malleolus and behind ankle to TA insertion, mid-foot and forefoot. Document ROM ankle joint, subtalar joint, mid-foot (abduction/adduction) and forefoot (extension / flexion 1st MTP joint) Palpate tibialis anterior (in front medial malleolus) and tibialis post (behind

med. malleolus). Assess power of tibialis posterior with single heel rise test: patient stand on small stool, faces wall, lift other foot and note heel raise of foot in question: hesitation /inability = positive test) Fig. 3. Perform Windlass test (dorsi flex big toe, medial arch should rise) (Fig 4).

Perform stability tests ankle (anterior draw test, ADT- hold lower tibia, foot plantar flexed, cradle heel in other hand and draw forward; no end-point is positive for ATFL rupture Fig. 5; inversion test - move heel into inversion, 10° greater than other side is positive for CFL rupture) Fig. 6.

Palpate pulses, check sensation and perform Tinel's test over posterior tibial nerve. Perform Simmond's test (patient prone, squeeze calf, no plantar flexion means TA is ruptured).(Fig-). Measure calf and mid-foot diameters.

Sports shoes

The ideal sports shoe should be comfortable, protect the foot and ankle from injury and possibly enhance performance.Shoes have caused problems since antiquity and more recently many of the forefoot problems have been related to poor shoe fit. (Sexy shoes / Painful feet).

There has been no convincing reduction in the incidence of injury from the use of athletic footwear. Perhaps we should return to barefoot (Zola Budd and Abebe Bikila preferred it and so do most school children) to restore plantar proprioception and reduce stress-related injuries. However sports shoes are here to stay (market-driven forces have seen to that) and its our job to make them work.

Current design concerns are:

· Shoe fit - female athletes are stuffing their feet into undersized 'male designed' sports shoes (female foot has larger forefoot / heel ratio so they need to use smaller heeled male shoe to get hindfoot fit and so cram their forefoot). Manufacturers are responding with 'female-designed' shoes to fix this problem.· Cushioning - transmitted impact forces may damage red blood cells (haemolysis), cause stress fractures (metatarsals) and alter hyaline articular cartilage. It seems that impact relieving soles will protect the foot and ankle.· Control - hyperpronation of the forefoot is a factor in injury, but this can be prevented with shoe wear (posterior medial arch

support) however the injury location shifts proximally to the knee (or distally to mid-foot). It is related to the hindfoot position with take off supination. Better hindfoot control is gained by high-top lace-up boots, or lateral heel flare. Side-stepping (or cutting) in sports where there is a rapid change in direction results in the lateral ligament complex. This is reduced in the barefoot or with a lateral heel wedge.1· Flexibility - Turf toe resulted from excessive flexibility of the American football shoe.· Foot / shoe / surface interface.

There are two interfaces here: the foot/shoe and the shoe/playing surface. Slip inside the shoe should be kept as small as possible (though not much research here). Interaction with the playing surface is easier to study and has received a lot of attention. Injury occurs when the deceleration forces exceed the breaking strength of bone/ligaments ( a sudden stop in sludgy snow) or from a slide (on icy snow resulting in collision).

Playing surfaces have changed from grass, clay, wood concrete, asphalt to synthetic turf (Astro-turf). The synthetics are easier to maintain, regulate and probably cause fewer injuries; they are characterized by degree of hardness, ground reaction forces, friction/traction, and energy loss, with loading and compliance. Increased traction (high co-efficient of traction with surfaces) may enhance performance but cause injury (as may slip from low co-efficient-but probably less likely). The cleating design of football shoes is critical to reduce torque and injury rate (change to soccer-style shoe or Tanel 360 shoe which has a circular cleat for synthetics and a central forefoot cleat for natural grass)

Sports shoes fall into 6 categories

(1) Running/training/walking(2) Court shoes(3) Field shoes - soccer/football - cleated/studded/spiked.(4) Winter shoes - ski boots(5) Outdoor sports - hunting(6) Specially sports - golf, cycling.

Details(1) Hiking boots need to be rugged, water resistant, good traction, firm heel counter. Climbing boots need inflexible soles. Exercise shoes need a light midsole with a firm heel counter, flexible soft upper and good shock absorption. Heel

height of 10-15mm.Running shoes for short distances-light heel; torsional stability in longer distances from slight wedge (especially curve running), semi pointed toe-box. Rules for spikes are 6 max for sole, 2 for heel (<2 5mm long and <4 mm wide). Shorter spikes for hurdles, sometimes spikeless or hard surfaces. Training flats (road work) need shock absorption, flexibility and heel counter stability with torsional stability (designated: light, heavy runners, heel strikers, anti pronation, light weight, rugged terrain) Traction variable by variable outsole thickness/tread.Throwing events use good grip leather/suede with spikes. Jumping events may use spikes but need heel cushioning and have 'jump foot' shoes (R or L).(2) Court shoes - Subject to heavy use. Tennis requires good lateral support, good tread pattern, ventilation. Basketball needs good ankle support, traction and a pivot point.(3) Field shoes. Use studs/spikes. Soccer need to feel the ball with soft upper. Football use cleats (but excessive traction may cause knee injuries). Need sturdy toe box and firm heel. Different shoes for different positions in US football (lineman versus backs versus place kickers). Rugby needs firm toe box.(4) Winter shoes: Skaters use leather uppers and firm heel counter. Injection moulded models. Skiing one piece injection moulded plastic foot outer shell. Modified for female foot. Cross-country are soft, low-cut, waterproof and good ventilation.(5) Specialty - cycle shoe similar to sprint shoe.

Ankle and foot sprains

Acute lateral ligament sprains

Inversion, with supination and plantar/dorsi flexion, causes injury of the lateral ligament complex. The most common sporting injury. Usually (2/3 of cases) the anterior talo-fibular ligament (ATFL, the weakest) is involved, sometimes the extra-articular calcaneo fibular ligament (CFL), seldom the posterior talo-fibular ligament (PTFL, the strongest). Those at risk are large athletes, those with pes cavus (high medial arches) and a history of similar injury. Prophylactic (S. Ankle) splints should be worn in high risk sports (basketball, netball, football). High top boots may help (Fig.7). There is immediate pain and (often marked) swelling with resultant anterior and inversion (tilt) instability. To judge the severity of injury, use the anterior draw test (Fig.); (Easier to perform in acute situation then inversion

test and will give more information). You may specify as Grade I-ATFL sprain (2/3 cases) (ADT - some laxity); Grade II-ATFL and CFL sprains (1/4 cases); (ADT and inversion tests some laxity). Grade III-ATFL, CFL and PTFL tears (both tests positive) or simply distinguish incomplete - with a firm end-point to anterior draw from complete - no end-point to anterior draw. Careful examination in the post-acute phase allows identification of the injured ligaments (after ankle RICE for 24 hours). Whether complete or incomplete, treatment is the same-non operative.X-rays are necessary to exclude fractures. Good talar dome views will exclude osteochondral fractures (ignore bony avulsion of the ligaments). Do not miss a high fibular fracture with syndesmotic injuries (Maisonneuve fracture). Stress x-rays are unreliable but possibly helpful in the chronic phase where the patient does not give a clear history of instability ('going-over' on the ankle). Treat in the acute stage with RICE, NSAIDs, ankle splint for 6 weeks (s-ankle; outer strap supports in swing phase and boomerang-shaped heel supports in stance phase with valgus and dorsal tilt), early rehabilitation with peroneal eversion exercises, water jogging, proprioceptive wobble board exercises. Some may become chronic. Elite athletes often elect for early surgical repair of complete ruptures (controversial but not unreasonable where 'wasted' period of 6 - 9 months conservative rehabilitation).Note: (Downhill) snow boarders may fracture lateral process of talus which maybe confused with lateral ligament sprain (often needs ORIF).

Chronic lateral ligamentous laxity

Unsuccessful treatment of acute lateral ligament injury may result in chronic lateral ligament laxity from 'stretched-out' ligaments. There is pain and tenderness over the antero-lateral ankle joint extending to the sinus tarsi, exacerbated by repeated inversion injuries on irregular terrain. Distinguish mechanical instability (positive ADT/or inversion test) from functional instability (feels unstable but is mechanically stable; a proprioceptive problem). There is anterior instability and excessive tilt. Treatment (Peroneal eversion exercises and wobble board) too often forces athletes to persist with months of unsuccessful physiotherapy. A quick effective lateral ligament reconstruction is better. (The Brostrom capsulorraphy with reinforcement from the inferior extensor retinaculum (Gould modification) is recommended here. lateral ligament complex is tightened-up and reinforced. Immobilized for 6

weeks and back to sport in splint in 3 months.)

Medial ligament sprains

Sprains of this type are rare. This is a strong ligament. Injury usually accompanies lateral ligament sprain or fractures, and must be differentiated from lesions of the nearby posterior tibial, FHL and FDL, tendons and syndesmotic injury. Carefully check for accentuated localized tenderness and consider ultra-sound examination (see tibialis posterior section). (posterior tibial tendon test invert plantar flexed foot against resistance; FDL test power of loop flexions toes against resistance; FHL test power of resistance of big toe); see diagnostic test syndesmotic injury, page 000.

X-rays with bone scan and CT may be necessary to exclude osteochondral fractures when there is severe, localized pain about the talar dome. Weight-bearing (WB) x-rays may be useful. An arthrogram in first week may show tear. Treatment is splinting and sometimes arthroscopic surgery if chondral damage.

Subtalar instability

Is a difficult entity to diagnose. This is really a component of lateral ligament injury (CFL torn) from inversion. There will be increased inversion compared to the other side. Special stress x-rays (Broden- invert heel and 40° caudal tilt) or I.I. may help. Treat either splint or in chronic cases as above with CFL reconstruction (as part of Brostrom operation.)

Syndesmotic ankle injury (high ankle sprain, distal tibiofibular diastasis)

Is a previously unrecognized, ongoing and painful 'ankle sprain'. In the professional athlete the condition probably results from an external rotation injury. There is marked swelling both sides of the ankle with tenderness over the interosseus membrane. Suspect where an ankle sprain takes a long time to settle down. Perform the squeeze test (compress upper tib/fib and distal pain occurs, Fig. 8) or abduction/external rotation tests (hold upper tib/fib and externally rotate/abduct ankle to reproduce pain) and check a mortise view (Fig.9) X-ray (>1mm reduction in the medial clear space AB or <10mm tibio fibular overlap CD). Late x-rays show calcification of the ligaments. Treat in NWB last for 4 weeks. If refractory use diastasis screw fixation and repair ligament (difficult to suture paint-

brush to paint brush).

Peroneal tendon injuries

The weak perineal tendons work hard, everting the foot (which wants to revert to gestational equinus) and maintaining the transverse / longitudinal arches of the foot. They are poorly anchored with a weak holding retinaculum. Forced dorsi-flexion of the everted ankle in skiing or football can produce tenosynovitis, tendinitis, tear, (partial or complete), subluxation or dislocation of these tendons (especially peroneus brevis which is closer to the bone). There is marked tenderness with reproducible subluxation or dislocation. Turn the foot in and out and note flicking of tendon behind the lateral malleolus. X-rays may show a rim fracture (lateral aspect lateral malleolus) Fig.10.Treatment: Strapping may help, otherwise decompression, repair, tenodesis to peroneus longus or early stabilization in the groove (because of high recurrence rate) is indicated. Must be a graduated return to sport over 4-6 weeks, with 'cutting' procedures and sprinting to be avoided for 6 weeks.

Posterior tibial tendon injury

Typically occurs especially in middle-aged women who are unfit as a result of chronic degeneration and in older athletes. The pathology is inflammation (tenosynovitis) or partial / complete rupture. There is pain and tenderness along the tibialis posterior tendon, with difficulty lifting the heel off the ground in the single heel-raise test pain/hesitation = tenosynovitis; not able to lift heel = complete tear). The arch is flattened and the foot pronated. Ultra-sound examination may secure the diagnosis.Treat with NSAIDs. Recommend a medial arch support with heel up for tenosynovitis and partial ruptures. Perform debridement/tenosynovectomy for refractory cases. Reconstruct complete tears (use the FDL).

Anterior tibial tendon injury

Spontaneous rupture may occur but is unusual. There is localized tenderness and weakened dorsi flexion. Treatment: surgical repair is important. Use either direct repair or tendon (extensor) transfer.


Introduction

Anatomy and biomechanics

Instability

Tendinitis and impingement

Internal derangements with the glenohumoural joint

Acromioclavicular joint injuries

Clavicle features

Outer clavicular osteolysis

Medical clavicular sclerosis

Sternoclavicular dislocation

Muscle ruptures

Biceps tendon injuries

Nerve injuries

Other conditions

Prevention of injury to the shoulder

Introduction

Because of its great mobility and intrinsic instability the should is the most vulnerable joint to injury in the body. It is required to provide a large range of movement with speed and force so the athlete can provide a top performance. We were never intended to be involved in all this above shoulder activity. Therefore little surprise that this joint is prone to a variety of injuries from the stresses being applied to the bones, chondral surfaces and the soft tissues. 8 -13 per cent of injuries sustained by athletes involve the shoulder.


The shoulder function consists of four separate joints-the glenohumeral joint(the main one), the acromio-clavicular, sternoclavicular joints and scapulo-thoracic. Disorders of any one of these may manifest as a dysfunction of the glenohumeral joint.

The glenohumeral joint (GHJ) is a ball and socket joint. The humeral head comprises about one third of a sphere. The articular surface has a medial angulation of 45 degrees to the shaft and is retroverted about 30 degrees. The glenoid fossa is pear shaped (radius of curvature is half that of the humeral head and so the area of bony contact is small). The glenoid labrum increases the depth of the fossa and increases the contact area of the humeral head and the glenoid. Ligamentous stability is supplied by the superior (major stabilizer) middle, and inferior glenohumeral ligaments and the capsule (Further stability from negative intra-articular joint pressures, the rotator cuff muscles and the coracohumeral ligament(Fig1)

The acromioclavicular joint (ACJ) is a diarthrodial joint which links the arm to the axial skeleton. There is little inherent bony stability. It has a variable fibrocartilaginous disc/meniscus. The capsule and the superior acromioclavicular ligaments stabilizes at physiological loads. Along with the coracoclavicular ligaments. the conoid and trapezoid.

The sternoclavicular joint (SCJ) has two incongruent articular surfaces with fibrocartilaginous disc forming two independent joints. It is stabilized by the interclavicular, anterior and posterior sternoclavicular ligaments and the costoclavicular ligament (rhomboid ligaments). The joint has three planes of motion. (The fulcrum is the rhomboid ligament, not the SCJ articulation.)Despite the low weight of the arm, (5% of body weight, i.e. 3.6 in a 72 kg man) high torque forces are generated by its long lever arm. The rotator cuff and other shoulder muscles generate movement and glenohumeral control. In throwing all the muscles of the trunk and upper limb work in a synchronized balanced manner to propel an object forward. Throwing action is divided into: cocking (or wind-up), acceleration and follow-through phases. Imbalance, fatigue, or damage to these structures may result in pain, tendinitis and/or instability (Fig.2).

Instability

Shoulder instability is common in sport. Apart from a frank, dislocation a wide range of symptoms result from variable degree of slipping of the shoulder. Partial dislocation is referred to as subluxation. This is not an insignificant injury to the glenohumeral joint, severe injuries occur from subluxed joints. These are 'instability events' (and potentially damaging to the joint), (95%) of shoulder instability is anterior/antero-inferior direction (other, directions include posterior/multidirectional.)

Anterior instability

Occurs when the arm is in abduction/external rotation and an anterior force applied on the shoulder joint, (fall on the outstretched hand or tackling a player with the arm out from the side, (rugby). May occur without an obvious traumatic event. Overhead sports, (baseball or tennis), cause a gradual stretch of the anterior capsule and symptoms of the shoulder slipping. Note hierarchy of support mechanisms controlling glenohumeral stability and so cascade of injury (see Table 1).

Table 1Minimal Loads

Joint Concavity

Finite Joint Volume

Adhesion/Cohesion

Joint Forces

Moderate Loads

Active

Co-ordinated

Cuff Contraction

Massive Loads Capsulo-ligamentous structures

Bony Supports

Symptoms of instability include: frank dislocation; slipping; pain with the arm in abduction/external rotation; apprehension when using the arm overhead or a 'dead arm' feeling with a tackle or overhead action. Clinical examination check ROM, strength, increased antero-posterior translation of the humeral head (Fig. 3) apprehension(Fig4) and relocation signs, note coincident tendinitis or labral tears and also signs of ligament laxity. (Hyper extend knee, elbow, MCP joints hand; flex wrist so hand touches forearm).The natural history(1) of the first acute anterior shoulder instability is now known. Recurrence in young patients (less than 22 years of age) is 62% (if participate in contact sports repeat instability is over 90%); Older patients (in 30-40 years old patients 25%). Over ten years period there is a 12% chance of a contralateral instability and a 20% incidence of arthritic changes on x-ray (9% moderate or severe). This arthropathy is thought not to be influenced by the number of dislocations or whether surgery has been performed.

Acute dislocation

Assess for any nerve or vascular injury x-ray the shoulder (AP + lateral in plane of scapula). Closed reduction can be performed in the emergency room using either Pethidine (50-100 mg IVI) Diaepham (5mg IVI) Nitrous2 oxide (entinox : 50% nitrous oxide / oxygen) or with an intra-articular injection

of lignocaine 1% (5cc). General anaesthesia may be required where there is excessive muscle spasm (or young male with huge shoulder muscle girdle).Techniques for Closed Reduction of the Dislocation Shoulder are described. Below (Table 2). The arm should be placed in a sling and physiotherapy organized after a 1 - 3 weeks. Younger patients have a high risk of recurrence; so for special sporting requirements consider an acute arthroscopic assessment and capsular/labral repair.

1 L. Hovelius 1987. Anterior dislocation of the shoulder in teenagers and young adults: five year prognosis. JBJS 69a, 393-399.2 E Sherry A Henderson J Cotton 1989. Comparison of Midazolam and diazepam for the reduction of shoulder dislocations and Colles' fractures in skiers on an outpatient basis. Aust. J. Sci Med. Sport.

Recurrent dislocation

If recurrent instability becomes a problem, options include: modification or avoidance of the precipitation event, a physiotherapy rehabilitation programme to strengthen the shoulder; or surgical reconstruction of the shoulder. Several of surgical techniques are used based on these correcting the pathology and those which tighten or use bone blocks to avoid dislocation. Correction of the pathology (Table 3) includes repairing the avulsed inferior glenohumeral ligament (Bankart lesion) and correcting any associated capsular redundancy (capsular shift) (preferred option in surgical management of the unstable shoulder). The success rate for surgery is 95%. Procedures which correct the pathology (i.e. anatomical reconstruction) are more likely to restore full range of motion. Especially for those involved in upper limb sports (requiring a throwing action e.g. baseball). Many of the non-anatomical reconstructions restrict external rotation and so restrict athletes. Types of shoulder reconstruction are described below.

Multidirectional instability (MDI)

Most shoulders show a variable degree of laxity (and is normal) where marked laxity this may become a problem. This may be insidious in onset or be related to a trauma. Important to differentiate laxity from stability. Laxity is a physical finding, whereas instability is the combination of symptoms and signs. The diagnosis of MDI, is based on finding least two directions (inferior plus either / or both anterior and posterior.) Patients have pain and weakness associated with a shoulder that subluxes inferiorly as well as anterior and posterior.

Take care in the evaluation of these patients. A small subgroup of MDI patients demonstrate a habitual / voluntary aspect to their problem. This group of patients should be evaluated for associated psychological problems and potential secondary gains. Surgical procedure will fail in this group.

Treatment focuses around rehabilitation. (Strengthening of the rotator cuff and scapula stabilizers, proprioceptive/biofeedback techniques and modification of activities.) Most will respond to physiotherapy. If necessary, surgery will include an inferior capsular shift with closure of the rotator capsular interval and tightening of the superior glenohumeral ligament. The results of surgery are 80-90% successful.

Table 2. Techniques for Closed Reduction of the Dislocated ShoulderTechnique Details/Comment

Scapular rotation Patient lies prone on table with injured arm hanging manoeuvre (Fig 5) off the edge of the table. The scapula is manipulated to open the front aspect of the joint so allowing congruence of the humeral head and the glenoid to be restored (inferior tip scapula pushed toward the spine). Elegant and effective.

Longitudinal traction Patient lies supine and the affected arm is slightly Technique abducted. Traction is applied to the arm with the (Fig5) foot (minus shoe) in the axilla or sheet around chest applying counter traction. Simple, historical and effective.

Stimson's technique The patient lies prone. Weight is applied to the arm with the affected should hanging off the edge of a table. Simple but lacks style.

Kocher manoeuvre The patient is supine. A sheet is applied around the patients chest. Traction is placed on the arm in slight abduction while the arm is externally rotated, adducted and then internally rotated. Old technique. Painful. May fracture or displace the neck of the humerus. Avoid.

Forward elevation manoeuvre The patient lies supine. The arm is gently elevated in the plane of the scapula up to about 160 degrees. Traction is applied in elevation with outward pressure on the humeral head. Simple and possibly effective.

Table 3. Types of shoulder reconstructions(1)

Anatomical

Type and Surgical details

Bankart Repair

The anterior detached capsule and labrum are repaired back onto the glenoid neck.

Capsuloraphy Stretched or redundant capsule is tightened by plication.

Inferior Capsular Shift Similar to a capsuloraphy but mobilization of the capsule extends inferiorly to take up redundant inferior pouch. Done in patients with very lax shoulders.

1 W J Mallon 1993. Shoulder instability. In Frymoyer (ed) OKU 4. AAOS. Rosemont Il. p297-302.

Non-Anatomical Reconstructions

Type Surgical details

Putti-Plan The anterior capsule and subscapularis muscles are divided, overlapped and tightened (Similar to converting a single-breasted coat to a double-breasted coat. Decreases external rotation of the arm.

Bristows Procedure The coracoid process is detached from the scapula and screwed onto the antero-inferior glenoid neck to give extra support to the shoulder.

Magnusen-Stack Procedure The subscapularis, capsule and a portion of the lesser tuberosity is detached fixed more laterally on the humeral; head. This tightens the anterior should structures decreasing external rotation.

Posterior instability

Posterior dislocation is uncommon (4% of all dislocations). Occurs from a fall; or violent muscle contractions as in an electrocution or grand mal convulsion. The diagnosis is often delayed or missed. There is pain and the arm is locked in internal rotation. The (antero-posterior) X-ray may look normal but beware check the axillary view (is diagnostic). If there is any doubt then a CT scan should be performed.]

Posterior subluxation

Posterior subluxation can occur from sports such as baseball. Suspect when the athlete experiences symptoms with the arm in front of the trunk. May then be associated with multidirectional instability. Clinical examination may reveal increased posterior glide, and symptoms reproduced on posterior load of the shoulder in 90° degrees forward flexion (Fig. ). The X-rays are often normal.

If there is a 'locked posterior dislocation', early recognition and reduction is essential. If the dislocation is long standing or a large portion of the humeral head damaged then open reduction with surgical reconstruction of the humeral head defect (by autograft, allograft or tuberosity transfer) is required. Where chondral damage has occurred, total shoulder replacement may be necessary.

In patients with posterior subluxations and associated multidirectional laxity, an intensive physiotherapy rehabilitation programme is required. Most patients will respond to this. If stability continues then surgical reconstruction is necessary (performed from an anterior or posterior approach). Anterior surgery consists of an inferior capsular shift and tightening of the superior glenohumeral ligament. Posterior reconstruction undertakes an inferior capsular shift only. In both cases the patient is immobilized in a neutral rotation brace for 6-8 weeks then placed on a graded rehabilitation programme extending over twelve months. No return to sports at least twelve months.

Tendinitis and impingement

The supraspinatus is vulnerable to inflammation as it passes under the coraco-acromial arch in the crowded space between the arch and the greater tuberosity. Tendinitis of the rotator cuff may occur from overload/fatigue of the cuff tendons, trauma, age related degenerative changes. The acromion may have a shape which increases the crowding of the cuff tendons here which leads to impingement Note: Tendinitis may occur in patients with very lax shoulders (the muscles are overworked to stabilize the humeral head). Therefore, it is important to beware of tendinitis in these patients (younger than 25 years) as this may be secondary to subtle (unrecognized) instability.

Typically there is pain over the anterior aspect of the shoulder with radiation into the deltoid (minimal at rest and rarely radiates down the arm or into the neck; aggravated with overhead and rotation activities). Night pain with waking indicates severe cases. Examination, tenderness is located over the greater tuberosity. Impingement signs are present (Fig 6 ). Biceps (tendinitis) provocation test may also be positive (Speeds test-pain with resisted forward elevation of strength arm; Yergason's test- pain with resisted supination of the flexed

elbow). The Acromioclavicular joint may be involved. Range of motion and strength are often normal, wasting does occur early. There is pain on loading the rotator cuff muscles. Weakness is due to inhibition from pain. Exclude cervical conditions which may refer pain into the shoulder; (where cervical irritation the shoulder posture is in a depressed or elevated position.)

The diagnosis of tendinitis is a clinical diagnosis. A plain X-ray is essential (include a supraspinatus outlet view) Next investigation is the impingement test. (5-10 mL of lignocaine is injected into the subacromial bursa, wait five minutes, there is then a significant decrease in pain on forward elevation of the arm to perform the impingement sign (Fig. 6). Ultrasound (in experienced hands) accurate in diagnosing full-thickness tears and impingement. Note all shoulders which are stiff, as in adhesive capsulitis, will show impingement on ultrasound due to tightness of the posterior capsule limiting the inferior glide to the humeral head, therefore, investigations should be considered in their clinical context. Arthrography will show cuff tears.

Treatment includes activity modification, NSAIDs and physiotherapy (consisting of stretching and strengthening of the rotator and scapular muscles). Most cases respond. If pain persists inject corticosteroid and local anaesthetic (½ ampoule celestone with 5mls 0.5% marcaine plain) into the subacromial space both diagnostic, and therapeutic. If conservative treatment doesn't help after 6 months, then acromioplasty (open or arthroscopic) is successful in 90% (Fig. 26).

Rotator cuff tears

Normal tendons seldom tear. For young patients if required a violent injury (instability of direct trauma) to tear the cuff. For older patient there is underlying degenerative changes in the rotator cuff so less trauma is required to disrupt it. With repetitive overhead use of the arm, (tennis or baseball), micro damage to the cuff can progress to a full-thickness tear.

The symptoms are similar to tendinitis. Pain is worsened by overhead activities, and at night. Weakness is present (however with full-thickness tears often there is a normal active range of motion). Only massive rotator cuff tears lose active range of motion. The long head of biceps may be torn as well.

Perform x-rays (may show an acromial spur and narrowing of the acromiohumeral gap where the tear is large) may need an arthrogram, ultrasound or MRI to confirm the diagnosis, extent of damage, atrophy of muscles and associated joint disease (note ultrasound is usually sufficient and cost effective).

Treatment in the young patients (less than 50 years) surgery (with acromioplasty and rotator cuff repair) is required as there is a risk of increase in tear size and deterioration of shoulder function. In older patients a short trial of activity modification, NSAIDs, physiotherapy and corticosteroid injection is reasonable. If pain then surgery with acromioplasty and rotator cuff repair is indicated.


Introduction


Ligamentous injuries and instability

Tennis elbow

Golfer's elbow

Osteochondritis dissecans

Panners disease

Little leaguer's elbow

Medial epicondylar fractures

Olecranon bursitis

Tendinous ruptures

Fractures and dislocations

Nerve compression syndromes

Intra-articular derangements

Introduction

The elbow is a difficult joint to examine diagnose and treat (not a frequent site of trauma and injury). Nevertheless the elbow is becoming better understood as more participate in throwing or overhead sports resulting in an increasing number of elbow problems requiring treatment.Overuse injuries in throwing or catching sports create most chronic elbow problems (may involve the ligaments, capsule, muscles or articular surfaces of the joint to impair function). Particular sports cause specific injuries around the elbow (Table 1).

Table 1. Sports specific elbow problems

Sport ConditionGolf Medial epicondylitisTennis Lateral epicondylitis

Baseball

MCL injuriesValgus extension overloadLittle leaguers elbow OCD Panner's diseaseUlnar neuritis/cubital tunnelAcute rupture MCLMedial epicondylitis

Gymnastics OCD

JavelinAcute rupture MCLPartial rupture MCLEpicondylitis


The elbow is a highly constrained hinge joint, (its stability is maintained by ligamentous, osseous and capsular structures) with a slight degree of varus/valgus and rotational laxity (3-5 degrees) throughout the flexion - extension arc.There are 3 articulations here (Fig. 1)· Ulnohumeral - allows 0-150 degrees flexion.· Radiocapitellar.· Proximal Radio-ulnar joints (radiocapitellar allows 75 degrees pronation and 85 degrees supination).Note: Most daily activity is done through a 100 degree arc of flexion and extension (usually 30-130 degrees) Forearm rotation occurs in an arc of 100 degrees, (usually 50 degrees supination and 50 degrees pronation). Any loss of this arc of movement may limit one's function.Elbow Stability. Ligamentous stability is provided by the medial and lateral ligamentous complex. (The relative importance of these ligaments depends on the position of the arm).Medial Collateral Ligament: has 3 parts. The anterior oblique ligament is the most important of these bands originating from the medial epicondyle and inserting onto the medial aspect of the coronoid process; The anterior band is the primary constraint to VALGUS instability and the radial head is of secondary importance (clinically, this is noted in throwing as the repetitive valgus stress can result in microtrauma and attenuation of the anterior oblique ligament).Lateral Collateral Ligament: has 3 parts and offers varus stability (rarely stressed in the athlete) The lateral ulnar collateral, the most important of these ligaments plays an important role in rotational instability, it originates from the lateral epicondyle and inserts onto the tubercle of the supinator crest of the ulna; Its function is to prevent Varus and Posterolateral rotatory instability of the elbow. The capsule serves as an important constraint to instability in full extension.Neurological anatomy. Neurological compression syndromes are common here due to the closeness of the nerves. The ulnar nerve is vulnerable within the cubital tunnel, posterior to the medial

epicondyle. The median nerve is anterior deep within the cubital fossa, the radial nerve is lateral and branches in the cubital fossa.

Ligament injuries and instability

Medial (ulnar) collateral ligament injuries (MCL)

From throwing sports where repetitive valgus stress results in small tears in the anterior band of the MCL and subsequent rupture. Occurs in javelin throwers and baseball pitchers (in throwing there is an enormous valgus stress on the elbow during the late-cocking phase so overloading the ligament leading to attenuation and rupture). Occasionally there is a single acute painful throw or a fall onto the outstretched hand.Examination reveals swelling and pain (localized to the medial side) and occasionally paraesthesia in the ulnar nerve distribution. Valgus deformity and elbow contracture may follow. Valgus stress testing with the elbow at 30 degrees of flexion displays increased laxity and pain. Incongruity develops between the olecranon process and its fossa with loose body formation at the medial side of the olecranon. X-ray's may show osseous bodies in the MCL or fluffy calcification at the tip of the olecranon.Treatment is rest, activity modification, NSAIDs and physiotherapy. If posteromedial pain continues then arthroscopy is necessary to debride the osteophytes. If there is chronic MCL laxity or instability then surgical reconstruction (primary repair or use palmaris longus is necessary.

Acute rupture of the MCL

Isolated tears of the anterior oblique ligament may occur in javelin throwers. The mechanism is almost pure valgus stress with the elbow flexed at 60-90 degrees. There is severe pain and a pop on the medial side of the elbow. Ulnar nerve symptoms may occur with ecchymosis about the elbow (48 hours later). If the diagnosis is in doubt stress tests or stress x-rays are useful . Acute

repair of the ligament is necessary.

Valgus extension overload

Seen in pitchers during the acceleration phase. (In the early phase of acceleration excessive valgus stress is applied to the elbow causing impingement). There results osteophyte formation posteriorly and posteromedially which can cause chondromalacia with loose body formation.

The pitcher presents with pain on pitching (early in the game) and are not able to let go of the ball. Pain over the olecranon fossa occurs in valgus and extension. X-rays show a posterior osteophyte at the tip of the olecranon (on lateral views).Treatment (should be started early) is increasing functional strength, heat and ultrasound. An osteophyte needs surgical excision).

Posterolateral rotatory instability(1)Differentiate from a frank elbow dislocation. Caused by a laxity or disruption of the ulnar part of the lateral collateral ligament which then allows a transient rotatory subluxation of the ulno-humeral joint (and secondary dislocation of the radio-humeral joint).

There maybe preceding trauma (dislocation or sprain from a fall on an outstretched hand). Previous surgery, radial head excision or lateral release for a tennis elbow, maybe the cause of instability.

There is a history of a recurring click, snap, clunking, locking of the elbow and a sense of instability that ones elbow is about to dislocate. Such stability episodes occur with a loaded extended elbow and supinated forearm. Examination, often unremarkable, should include the 'Lateral Pivot Shift' (Posterolateral rotatory apprehension test)(Fig 2- Performed with patient supine, preferably under general anaesthesia; The elbow is extended overhead and the forearm fully supinated; A valgus and supination force is then slowly applied to the elbow going from the extended to flexed position; This results in

subluxation of the ulno-humeral joint and radio-humeral joint ).

On X-ray the joint will look normal (unless taken with the joint subluxed) so the diagnosis is made from history and after above test. When symptomatic surgery is required (re-attach the avulsed lateral ulnar collateral ligament or reconstructing it (with a tendon graft).

Tennis elbow (lateral epicondylitis)

A lateral tendinitis which involves the origin of Extensor Carpi Radialis Brevis. It is related to activities that increase tension and stress on the wrist extensors and supinator muscles (not all activities include tennis. It occurs between the ages of 35-55 years with pain localized to the lateral epicondyle especially after a period of unaccustomed activity (such as tennis 3-4 times a week). The pain is worsened by movements such as turning a door handle or shaking hands. Examination reveals pain localized to the lateral epicondyle and distally. Typically aggravated by passive stretching the wrist extensors or actively extending the wrist with the elbow straight (Fig.3 ).X-rays are often normal (to exclude OA, LB or tumour). A bone scan will show increased uptake about the lateral epicondyle. An ultrasound or MRI will show degeneration within the belly of ECRB. The differential diagnosis includes: posterior interosseus nerve entrapment ( has a more distal localization of the pain and associated weakness); radial tunnel syndrome (pain distal and exacerbated by resisted extension of long digit, i.e. ECRB); OA/LB/Tumour.It will resolve over a 10-12 month period but there is a 30% recurrence therefore treat comprehensively(1) with rest, activity modification, NSAIDs, heat, ultrasound, phonophoresis with 10% hydrocortisone cream, brace (counterforce effect), eccentric muscle

strengthening, modify tennis handle (usually too large) or tennis stroke (occurs in back hand stroke). injection of cortico-steroid (no more than 3, just below ECRB, anterior and distal to the epicondyle), and then surgery (symptoms >12 months, release and excise ECRB, note Nirschl scratch effect). Return to sport when strength 80% back or after 4 to 6 months.


Introduction

Biomechanics

Assessment of Injury

Management of an isolated hand injury

Fractures

Dislocations and collateral ligament injuries

Jersey finger

Wrist fracture

Carpal instabilities and ligamentous injuries

Triangular fibrocartilage complex tears

Soft-Tissue Wrist Pain

De Quervains tenosynovitis

Wartenberg's syndrome

Intersection syndrome

Scaphoid impaction syndrome

Ulnar abutment pain

Nerve compressions

Chronic compartment syndrome

Introduction

The hand and wrist are frequently injured in sport. Careful assessments and investigations will improve diagnosis and management. The essential functions of the hand are touch, firm and precise grip. (The thumb opposes the fingers and provides this precise grip). The wrist is the stable platform for the hand and so fine-tunes grasp. Hunter, tool-maker(1), surgeon and athlete all depend on their hands.

1. Were our big - brained ancestors The first tool-makers or were they some distant, dead end, small - brained vegetarian cousins? It's not that clear.Ann Gibbons 1997 Tracing the Identity of the First Tool-Makers. Science 276, p32

Biomechanics

Biomechanics and function are inextricably linked. (This interplay nowhere more evident than in the hand). Tendons, intrinsic muscles, nerves and vessels form on intricate, yet robust unit capable of delivering knock-out punch or putting the ball to the cup.

A knowledge of surface anatomy is important (Fig.1). (Know some more common anatomic variations, e.g. Flexor digitorum superficialis to the small finger is absent in a significant number of people, an extensor digitorum manus brevis may be confused with a ganglion).

Note that a relatively small amount of oedema in the finger is enough to significantly restrict movement (especially at the PIP joint, see Fig. 2).

Assessment of injury

What is the chief complaint? Either 'It doesn't feel right; it doesn't work right; it doesn't look right.' What was the position of the hands and fingers at the time of injury? Such an understanding of the mechanism of injury with the chief complaint will be enough to secure the diagnosis (confirmed by exam and x-ray). The team doctor may witness the injury as it occurred.

Check the skin and nails, each joint, (ligaments for stability, mobility of joints). Nerves (check sensation and motor supply), vessels (pulses, branching of nail bed) and bones (provide stability).

Ask the patient to localize (point with one finger, to one spot!') the site of the problem. (The site of maximal tenderness). The exam should proceed in an orderly sequence. Look, feel, move. Always compare sides.

Look. Inspect the dorsal and palmar surfaces. Look from the side, above and end of on. Note the position of wrists, hands and fingers. (Any abnormal posture suggestive of a fracture, ligament or tendon injury). Note of swelling, lacerations, bruises and sweat patterns.

Feel. Palpate the area of concern, seek sites of tenderness, instability, masses, etc. Assess sensation and circulation. Perform the relevant provocative manoeuvres. Assess grip and pinch strengths.

Move. Ask the patient to make a complete fist and fully extend , abduct and adduct all fingers and both thumbs. Check wrist dorsiflexion, palmarflexion, radial and ulnar deviation, pronation and supination.

X-rays (specify views and sites, a minimum of two views at right angles). Special views are useful in assessing wrist injury (PA clenched fist for scapholunate gap, carpal tunnel for (hook and hamate fracture and pisotriquetral views). At the very least: PA views a neutral, ulnar and radial deviation and direct lateral are necessary.

CT scanning will provide additional anatomic information in trauma to the wrist, (where difficult or unusual fractures, fracture/dislocations around the base of the metacarpals and carpus).

Bone scans (where, but not what) are useful in the assessment of chronic wrist pain.

Ultrasound ('operator dependent') can localize non radio-opaque foreign bodies, and give much valuable information about soft tissue masses, tendons and ligaments.

MRI may be of value in assessing the triangular fibrocartilage complex. (TFCC.).

Management of an isolated hand injury

Initial Priorities· Stop bleeding (direct pressure)· Relieve pain (digital/wrist block)· Assess injury (and splint)

Path of Recovery· Pain relief· Protection· Physiotherapy

A digital, or wrist block is the best way of relieving pain (Lignocaine 2%, without adrenaline, in doses not exceeding 5mg/kg, any nerve injury must have been assessed and documented prior to the nerve block).

Splinting the injured part is a simple (sadly often forgotten) way of providing effective and rapid pain relief. Splint as it lies or in the 'safe' position, (the wrist in about 30º extension, metacarpophalangeal joints 70-90º flexed, and the interphalangeal joints fully extended. The thumb, if included, is held parallel to the index finger). In this position the collateral ligaments are at their longest.

The coach can correct faulty technique and advise the medical team on the demands of the sport. But the patient is primarily responsible for their own recovery. Only the patient can do and carry out the given advice.

Pain relief, protection and physiotherapy are the three 'Ps' on the path to recovery.

Pain relief. Use ice, crepe and elevation (to reduce pain and swelling). Analgesics are used. Ice, heat, laser and TENS will also reduce pain.Steroids (betamethasone *'Celestone'* or methylprednisolone *'Depomedrol'* have no place in acute injury. Useful in chronic inflammatory conditions (only two or three injections be given in one area). Complications with prolonged use included skin atrophy, fat necroses, infection and tendon rupture.Athletes (under pressure to get back into competition) may request a 'pain killing injection'. The injection of local anaesthetic is not indicated. If the hand is too painful to stand up to a the demand of competition it is not 'ready for them'.

Protection. Continue splinting from acute phase of injury if

necessary to stabilize and protect. (Allows protected movement (buddy taping' to a healthy digit is easy and useful), apply tape so as not to interfere with joint movement, be careful when buddying an injured small finger to the right ring finger as a deforming rotatory forces may be applied to the injured digit). Dynamic splinting is best and often used in combination with static splints (at night). (S-Thumb will protect thumb or wrist). Surgery may be necessary to get stability and protection.

Physiotherapy. Early active movement should begin as soon as possible. When pain settles, stability is established, and movement returns, stretching and strengthening are started. Any impediment to movement should be removed. (Pain, instability and oedema).Oedema is lessened by movement, elevation, ice, and pressure from elastic bandages (Coban or similar) or tailor made gloves. Massage, laser, and intermittent positive pressure (Masman pump) will help.

Fractures

The biology and biomechanics of fracture and soft tissue healing are no different in the athlete. (Athletes do not heal any quicker because they seek the advice and treatment of a 'sports doctor'). In general, fracture union in the upper limb occurs in about six weeks (in the adult, and about half this in a child, fracture consolidation takes twice as long). What is different is the attitude to injury. The demands of competition (especially at the elite level) may result in the athlete returning to training and competition too early, (so running the risk of further injury). Financial concerns may bear on this decision to return too early. The athlete will make the ultimate decision. It is the role of the sports medical team to advise what the risks are and how they may be minimized.

The clinical signs of fracture are important (pain, swelling, deformity and loss of function). Diagnosis is confirmed by x-ray. Early movement is the key for a swift return to full function (so the fracture must be of a stable pattern, or be rendered stable by splinting or surgical fixation). Outcomes deteriorate if active range of motion is delayed beyond three weeks.

A fracture is reduced under appropriate anaesthetic by closed or open means and rendered stable. (Confirm by x-ray and repeat

one week post injury and later as necessary). If the fracture cannot be made stable by splinting, surgical fixation is necessary. In general, displaced fractures involving joint surfaces will require reduction and surgical fixation. Note the called 'clip' or avulsion' fractures, the bony equivalent of a tendon or ligament rupture, will usually require surgical repair.

Distal phalanx fractures

These result from a direct blow, often with the finger being 'crushed' between the bat and ball. The hallmark is a subungual haematoma. The nail plate maybe lifted out of the nail fold, suggesting that the fracture was, displaced and that a significant injury to the nail bed has occurred. A painful subungal haematoma under pressure may be relieved by drilling the nail plate with a sterile 19 or 19G needle, x-rays should then be taken as such (surgical cleaning of the fracture site, with accurate repair of the nail bed, magnification, and fracture fixation where appropriate give the best result; some surgeons feel a haematoma involving more than 25% of the nail plate is an indication for its removal to allow nail bed repair).

Bony mallet

Catching a finger on the ground ball, or opponent may result in avulsion fractures of the extensor tendon (bony mallet) or less commonly avulsion of the flexor tendon (this latter one is more serious and usually less recognized). Almost always require surgical treatment. Note: occasionally the tendon will pull away from the bone chip and be found in the palm.

The bony mallet (if no more that 30% of the joint surface is involved and no joint subluxation) is treated in a hyperextension splint (maintain for at least 6 - 8 weeks,) Instruct patient in skin care and changing splints.

Middle and proximal phalanges, metacarpals

Transverse fractures of the middle phalanx (distal to the insertion of flexor superficialis) result in extension of the distal fragment, those proximal to its insertion are flexed. Transverse fractures of the proximal phalanx usually result in the interossei flexing the proximal fragment. Transverse fractures of metacarpals tend to have the distal fragment flexed by the long flexors. Reduction and neutralization of the deforming forces may be possible using buddy and extension block splinting.

However short oblique, and spiral fractures of the phalanges and metacarpals may shorten/rotate and so require surgical fixation. Rotation is assessed with the fingers in flexion. The fingers should not cross and the tips should individually point to the tubercle of the scaphoid.

'Boxer's fracture'Boxers fracture (a fracture of the neck of the small finger metacarpal and a result of bar-room brawling) is usually best treated in a resting splint with the hand in the safe position until pain and swelling subside (7-10 days) followed by active mobilization. Such fractures generally do not require fixation despite what appears to be marked x-ray deformity.

Chapter 11

Hip, Thigh, and Pelvis

Introduction Biomechanics Contusion of quadriceps Myositis ossificans traumatica Quadriceps strain and ruptures Avulsions of the iliac spines Hamstring strains Ischial apophysitis Groin strains Hip pointer and fracture iliac crest Iliac crest apophysitis and avulsion Trochanteric bursitis and snapping hip Hip strain Conjoint tendon strain Osteitis pubis Nerve entrapment Labral tears Stress fractures Fractured hip; acute slip of the upper femoral epiphysis (SUFE) Dislocation of the hip Fractured femur and pelvis Hip arthroscopy Avascular necrosis femoral head Osteoarthritis

1 Ireland J 'The Hip, Thigh and Pelvis' in Sherry E and Bokor D (eds). Manual of Sports Medicine, Chapter 13. GMM, London, 1997.

Introduction

Injuries of the hip, thigh and pelvis are not that common from sport. They may be subtle in presentation and diagnosis is difficult or catastrophic with serious immediate and long -term consequences (e.g. hip fracture or pelvic fracture with shock).

Biomechanics of the hip

The hip is a ball and socket joint with simultaneous motion in all 3 planes (up to 120° of flexion, 20° of abduction and 20° of external rotation). The joint reactive forces are 3 to 6 times body weight due to contraction of the large muscle groups about it; this is increased to with jumping or running.

The acetabulum has a fibrocartilaginous rim (labrum) to deepen it and so add further stability. The postero-superior surface of the acetabulum is thickest to accommodate weight-bearing. the neck forms an angle of about 125° with the shaft and is 20° anteverted. The hip capsule drops down across the front of the neck but only part-way at the back. It is reinforced by three ligaments (the ilio-femoral ligament of Bigelow is the strongest). The major blood supply to the head is from the medial circumflex branch (of the profunda femoris) which is at risk from fractures of the neck of femur and dislocations.

Contusion of quadriceps (cork thigh, Charley Horse)

The result of a direct blow during contact which varies from mild to severe. Often worse when the muscle is relaxed and occurs in the musculotendinous junction of the Rectus femoris (central position of the quadriceps).

Clinical features There is pain, stiffness, a limp, and progressive swelling with bruising. The pain is increased by resisted knee extension and hip flexion. Due to bleeding into the soft tissues symptoms becomes worse over the subsequent 48 hours.Classified according to that of Jackson and Feagin (1) (see also Table 1)Table 1. Classification of contusion quadriceps

MildLocalized tenderness in the quadriceps, knee motion of 90 degrees or more, no alteration of gait. The athlete is able to do a deep knee bend.

ModerateSwollen tender muscle mass, less than 90 degrees of knee motion and antalgic gait. The athlete is able to do knee bends, climb stairs, or arise from a chair without pain.

SevereThigh is markedly tender and swollen and the contours of the muscle cannot be defined. Knee motion is less than 45 degrees and there is sever limp. The athlete prefers to walk with crutches and frequently has an effusion in the ipsilateral knee.

Treatment: There are three phases in the treatment.(2) Measure thigh diameter and follow to exclude small chance of compartment syndrome developing The first is limitation of motion to minimize haemorrhage (with rest, ice, compression and elevation). The leg is maintained in extension and quadriceps isometric exercises are allowed. Do for 24 hours, in mild contusions, 48 hours in severe. A more recent study otherwise keep hip and knee flexed (probably as effective).. D W Jackson, J A Feagin. 1973. Quadriceps contusions in young athletes JBJS 55A, 95-105.2. B. Rooger, S Bergston, G. Hagglurd. Acute compartment syndrome from anterior thigh muscle contusion: a report of eight cases 1991. J. Orthop. Trauma 5, 57-59.The second is the restoration of movement. This depends upon the condition of the quadriceps stabilizing and the patient being pain free at rest. Use continuous passive motion and gravity assisted motion. Supine and prone inactive knee flexion is encouraged along with isometric quadriceps exercises. Once a pain free passive range of motion of 0 to 90 degrees is achieved, and good quadriceps control, to static cycling with increasing resistance. At the end there is ROM >90° and normal free gait (without a crutch).The third is functional rehabilitation with progressive increasing resistance exercises builds strength and endurance. Must always be pain free.

Myositis ossificans traumatica

A severe contusion or tear in the quadriceps with haematoma followed by acute inflammation. Fibroblasts then form osteoid. Specific risk factors have been identified(1).

o Knee motion <120°.o Injury from football.o Previous quadriceps injuryo Delay in treatment ( > 3 days).o Ipsilateral knee effusion.

Clinical features - pain is over the front of the thigh along with a fluctuant mass which forms into a hard mass at the two to four weeks. (May resolve after six months if the injury is low grade and in the musculotendinous region).

Treatment as for contusion of the quadriceps. Aspiration or open drainage of the haematoma may be necessary. Femoral nerve blocks, NSAIDs and radiotherapy have been used.

Quadriceps strain and ruptures(1)

The result of a severe contraction when either accelerating or kicking (usually the rectus femoris and distal in the thigh).

Clinical features are localized tenderness or a palpable defect (Fig 1). The pain is exacerbated by resistance of hip flexion in extension and full knee flexion in a prone position. MRIs show a high signal on a T2 weighted image.

Differentiate from an L3 nerve root lesion (pain is in both mid-lumbar back and leg); made worse by straight leg raising).Treatment as for quadriceps contusions.

1. J B Ryan, J H Wheeler, W J Hopkinson et al. 1991 Quadriceps contusions west point update Am J Sports Med 19, 299-304.

Avulsions of the iliac spines

The mechanism of injury is a sudden violent contracture of the rectus femoris muscle, (occasionally the sartorius muscle seen in soccer players. Players tend to be in their mid teens.

Clinical features - include severe pain point tenderness and bruising (sometimes dramatic) diagnostic. Treatment includes rest, ice, compression and elevation. If there is persisting functional impairment then surgery may be necessary to fix the apophysis or avulsed fragment. Sometimes the bone fragment needs to be excised (at later date).

Hamstring strains

In the late swing phase of the gait cycle, hamstrings decelerate the limb. with sudden acceleration from the stabilizing flexion to active extension, strain is put on the hamstring muscles. This injury is most likely to occur with sudden hamstring contraction in athletes when they are cold or have not done adequate stretching. Common situations are at the starting blocks, sprinters at take off, (or high jumpers and long jumpers) an sudden acceleration or resisted extension by football players(Fig 2).The short head of the biceps femoris is most commonly affected. Occasionally dystrophic calcification is seen.

The patient may describe a twinge or a snap and localize an area, (such as the short head of the biceps). Swelling and a palpable defect are common.Treatment includes rest, ice, compression, elevation and physiotherapy (local cryotherapy and ultrasound). A stretching programme is commenced once pain has subsided. Recovery is from days to week (depending upon the severity).

The key to treatment is to remedy poor training techniques and improve flexibility. The athlete must carry out an adequate warm-up and stretching programme prior to a return to sporting activities. The significant imbalance

between quadriceps and hamstrings needs to be overcome, and adequate return hamstring strength before returning to sport. A firm elasticized support is useful.

Re-injury may occur with longer recovery; therefore exercise good judgement about when to return to sport.


Introduction

The goals of training nutrition

What is 'ideal' body shape and composition?

Reducing weight and body fat

Increasing muscle mass

Energy requirements for athletes

Protein needs of athletes

Vitamins and minerals

Iron

Calcium

Supplements in sport

Optimizing training and recovery

Practising nutritional strategies during training

Goals of the competition diet

Preparing adequate fuel stores

The pre-event meal

Fluid and CHO intake during exercise

Recovery after exercise

Summary

Introduction

Why is sports nutrition important and who is it important for? It is easy to understand the search for a competitive edge in the elite world of sport. In many events, the margin between winning and losing is measured in millimetres and hundredths of seconds, and the stakes include international fame and considerable amounts of money. A number of prominent sports scientists have suggested that at this level, where genetics, training, equipment and motivation are all equalized, nutrition might provide the vital ingredient in success.

However, it is clear that recreational athletes are also interested in sports nutrition, as shown by the recent boom in the marked for specialized sports drinks and sports bars. Although some people consider that special sports nutrition strategies are relevant only to the elite athlete (or that these specialized sports foods are a waste of money for the non-elite sportsperson), it is important to realize that the fundamentals of exercise physiology apply to sporting activities, regardless of the talent of the athlete involved. For example, sweat losses and carbohydrate needs are created by muscular activity, whether it be undertaken by Michael Jordan or Joe Public. While for recreational athletes, the rewards of sports nutrition strategies are likely to be the satisfaction of improving 'personal bests' or achieving personal goals, the spin-off of better safety and enjoyment of exercise activities may be an important factor in encouraging population participation in exercise. Finally, since many of the principles of sports nutrition concur with population dietary guidelines, the interest in sports nutrition may independently help to improve the general health and nutritional status of the population.

Sports nutrition is underpinned by the sciences of exercise physiology and biochemistry, and aims to supply the body with the nutrients needed to adapt to a training program, to perform optimally during competition and to recover quickly after exercise. However, sports nutrition also involves the art of translating nutrient needs into foods and eating practices that are compatible with the busy schedule and commitments of an athlete's lifestyle. This chapter will summarize the current guidelines for achieving both the science and practice of 'eating to win'.

The goals of training nutrition

The purpose of training is to prepare the athlete to perform at

their best during key competitions, and inmost situations the time and demands of this preparation far outweigh those of competition. Therefore, it is the everyday or training diet of the athlete which has the greatest impact on sports performance. The athlete shares the population nutritional goals of meeting nutrient requirements for immediate health, as well as adopting dietary strategies to reduce the risk of developing Western disease patterns in later life. Additionally, they should be able to participate in the enjoyment and social interaction that is provided by food. However, the athlete must also meet special goals of sports nutrition during the training phase including:

- to achieve a body size and composition that is ideal for performance in the athlete's sport- to meet additional demands for energy and nutrients that arise from the training program - to undertake dietary strategies that optimize performance during training sessions and enhance recovery after the session- to practice any competition nutrition strategies in advance so that these can be fine-tuned for success.The importance and the details of these goals will vary from sport to sport.

What is 'ideal' body shape and composition?

The size, shape and composition of the body are important determinants of performance in many sports. In some sports, weight divisions or limits are set to encourage fair competition between opponents of equal size and strength. These sports include weight lifting, boxing, judo, light weight rowing and horse racing. In other sports, a low weight and/or low body weight level is a factor in successful performance. This may be to increase the athlete's 'power to weight' ratio, or to reduce 'dead weight' that must be transported over long distances (e.g. in distance running, road cycling or triathlons) or moved against gravity (e.g. jumping events, hill cycling). In some sports, the aesthetic appeal of a lean body provides favourable characteristics for judging (e.g. in body building, gymnastics, figure skating), although this is usually combined with the biomechanical advantages of being small and light (e.g. in gymnastics).

In many situations, the athlete achieves a suitable body size and shape for their sport as a result of the combination of the genetics which have 'selected' them to excel in that sport in the

first place, and their training programme. However in other situations the athlete may desire to alter their physique - typically to lose body fat or to gain muscle mass.

Reducing weight and body fat

Sometimes the need to lose body fat is desirable and achievable. Some athletes become overfat due to poor dietary intake (e.g. as a result of poor nutrition knowledge or erratic eating patterns due to travel) or due to a period of a low energy expenditure (e.g. during the off-season, or while injured). These athletes can be assisted by changes to nutrition, training and lifestyle to regain their 'optimal' body fat level. In general, body fat losses are achieved by a sustained program of moderate energy restriction and appropriate training/increased energy expenditure.

However there is much concern about athletes who seek to achieve body weight and fat goals that are extreme and unnatural. There is considerable pressure on athletes in many sports to achieve very low body fat levels in the belief that 'less is better', or to achieve body fat and weight standards that are arbitrarily set by coaches or other authorities. These practices do not allow for individual variability in physique, nor do they encourage safe and healthy methods to achieve loss of weight and body fat. This situation is particularly true for female endurance athletes, whose desired body fat levels often seem below the 'natural' level for the individual, despite their heavy training programme. The problem is compounded in the case of females in 'aesthetic' sports (e.g. gymnasts and figure skaters), where training is skill-based and energy balance must be changed primarily through energy restriction. Problems also occur in weight division sports where the tradition is to compete in a weight class which is considerably below 'normal' training weight, and to 'make weight' by 'dieting' to reduce body fat levels, superimposed by acute dehydration during the day(s) prior to the event. Performance in 'weight making' sports is likely to be impaired due to the effects of fuel depletion and dehydration. However, in the larger view there appears to be an increased risk of disordered eating and eating disorders among athletes in sports in which low body fat levels are emphasized.

It is a challenge of sports nutrition to assist athletes to set and achieve body weight and body fat goals that are truly 'ideal'. This should include the notion of individuality, allowing the

goals to be set according to the athlete's history and realistic potential. Studies of elite sports show that, although there is a 'typical' physique that seems favourable for performance, there is considerable variation in the physique of well-performing athletes. The athlete should be aware of the disadvantages of fad diets and of extreme fat/weight loss techniques. They should also recognize that there may be penalties for achieving very low body fat levels, at least when it does not seem to be penalties for achieving very low body fat levels, at least when it does not seem to be the athlete's natural physique. These include hormonal, physiological and psychological disturbances and may result from the low body fat level itself, as well as from the methods involved in achieving it (i.e. restricted eating, overtraining, stress). An 'ideal' weight and body fat level for any athlete should guarantee consistently good performances over a long term period, promote good health, and allow the athlete to consume a diet of sufficient energy and nutrients that allows all goals of training to be achieved. The need for individualized and expert advice on management of body weight and fat is the most common reason for an athlete to seek the services of a sports dietitian.

Increasing muscle mass

The other physique change desired by athletes is an increase in muscle size and strength. This is principally achieved by a suitable resistance training programme and genetic potential; however an adequate energy intake and usually, a positive energy balance is required. Although the protein needs for optimal muscle gain remain an emotive area for many athletes (and scientists), the primary dietary requirement for gain in muscle mass is energy. For some athletes, dietary counseling is required to provide strategies for increasing energy intake in an already high energy diet or in a busy timetable.

Energy requirements for athletes

The energy requirements of athletes vary markedly and are influenced by the size of the athlete, the need to lose or gain weight, growth, and the training load (frequency, duration and intensity). Dietary surveys of athletes find that male athletes generally report energy intakes varying form 10-25 MJ/day (2500-6000 (Cal/day) over prolonged periods.

However, while the energy requirements of female athletes might reasonably be - 20-30% lower than their male counterparts, principally to take smaller size into account, some surveys of female athletes often report an 'energy imbalance' whereby reported intakes of 4-8 MJ/day (1000-2000 Cal/day) are lower than expected and sometimes do not seem to cover the costs of the training programme itself. There appears to be no physiological explanation for this. Rather, systematic under reporting of food intake or 'restricted' eating during the period of the food diary due to concerns about body fat levels are suspected.

Protein needs of athletes

The protein requirements of athletes are increased by training. This results from the small contribution of protein oxidation to the fuel requirements of exercise as well as the protein needed to support muscle gain and repair of damaged body tissues. While athletes undertaking recreational or light training activities will meet their protein needs within population protein RDIs, a guideline for increased protein intake for heavily training athletes, both endurance and strength-training, has been set at 1.2-1.6 g/kg BM/day. These targets are easily met within the increased energy requirement enjoyed by athletes who undertake such training. Indeed most dietary surveys show that athletes who eat a typical mixed diet report protein intakes within or above these goals. Despite this evidence, many body builders and weightlifters eat unnecessarily large amounts of protein-rich foods or buy expensive protein supplements.


Introduction

Skin infections

Sports-related allergic and irritant dermatitis

Dermatological manifestations of physical, cold, and electromagnetic injury

Heat and cold related skin disease

Ultraviolet-related skin disease

Exacerbation of pre-existing skin disease

Dermatological effects of anabolic-androgenic steroids

Introduction

The skin plays an important role in protecting the body from noxious external stimuli such as mechanical forces, temperature changes, and harmful chemicals. It is no surprise, therefore, that cutaneous disorders are an important factor in every athletic specialty. Sports dermatology is concerned with skin disorders related to athletic activity, manifesting either as a primary disorder or as an exacerbation of a pre existing dermatological dermatosis. Sports dermatology is an enlarging field and this chapter summarizes some of the more commonly encountered problems.

Skin infections

Fungal infections

Dermatophytic fungi live in the stratum corneum (most superficial epidermal layer) and can cause superficial infections. Tinea pedis or 'athlete's foot' affects the interdigital and lateral areas of the feet and is characterized by pruritis, scaling, and occasional soreness. The classic 'wet form' presents with white macerated scale, fissures, and occasionally with vesicles and bullae. Less commonly a 'dry form' or 'moccasin foot' is seen as a dry, rough, diffuse white scale affecting the sole. The problem is often bilateral and the toenails may also be involved (manifest by discolouration, thickening, crumbling and Subungual scale of one or more toenails). Tinea pedis is a chronic disorder and patients may be afflicted for decades. Infection occurs by person-to-person or by contact with infected fomites such as a towel or floormat. It is undoubtedly influenced by the microenvironment of the clad foot, and factors which exacerbate the condition include a moist, warm environment; a sweaty foot enclosed in a non-absorbent sock and occlusive shoe such as a 'trainer' is a likely target for tinea pedis. Secondary bacterial infection is sometimes seen and may present as cellulitis, lymphangitis, or inguinal lymphadenopathy. The diagnosis of tinea pedis is confirmed by examining scrapings of keratinous debris in a 10% potassium

hydroxide (KOH) preparation and observing the characteristic hyphae. Culture permits identification of the causative fungus (usually Trichophyton rubrum, T. mentagrophytes, or Epidermophyton floccosum).

The differential diagnosis includes pompholyx, pustular psoriasis, pitted keratolysis and allergic contact dermatitis to shoes; a positive skin scraping however does not necessarily exclude these dermatoses, as a superficial dermatophyte infection may be superimposed upon an area of already broken skin. Treatment Acutely inflamed 'wet' forms of superficial fungal infections should be treated with a combination of shooting antiseptic soaks or paints (e.g. Castellan's) and topical antifungals. Soaks should be lukewarm and contain potassium permanganate 1 in 10 000 and the feet immersed in the solution for 15 minutes three times daily. Effective topical antifungals include the newer imidaoles such as miconazole, econazole or clotrimoxazole in a cream or tincture base; these should be applied twice daily for approximately two weeks. Careful attention should be given to avoidance of exacerbating factors such as sweat, heat, and occlusion. Socks should be cotton or wool, and preferably changed once or twice during the day. Footwear such as thongs or clogs should be worn while using communal showers or change rooms. Athletes should alternate pairs of sneakers or shoes if possible to allow airing in between periods of wear. Infection of the nails is an indication for oral antifungal therapy as dermatophyte in the nail are relatively resistant to topical agents. A new allylamine drug, terbinafine, can achieve a mycological cure of toenail onychomycosis in 70-80% of patients following twelve weeks of therapy. Other oral agents used include griseofulvin, ketoconazole and intermittent itraconazole. Although generally safe agents, ketoconazole is contraindicated in patients with hepatic disorders and can interact with other medications, for example, warfarin. Itraconazole has fewer hepatic side effects but is considerably more expensive than other oral antifungals. Amorolfine 5% nail lacquer can be applied to affected nails once or twice per week and has shown to cure approximately 40-55% of patients with toenail onychomycosis.

Other fungal infections include tinea cruris, tinea versicolour and tinea incognita.

Tinea curis ('jock itch')Commences in the groin folds and extends out in an annular or circular fashion with a scaly, inflamed border. Hyphae can also be identified on KOH preparation of scale taken from the active

advancing border. Treatment of tinea cruris is with oral griseofulvin and concomitant topical treatment with one of the newer imidazole creams.

Tinea versicolourNot actually a dermatophyte infection but is due to the saprophytic yeast Pityrosporum orbicular which develops into is parasitic fungal form Malasezia furfur. This transformation may be provoked by humidity, ambient heat, as a result of exercise, secondary to diabetes mellitus or iatrogenic immunosuppression e.g. systemic corticosteroid treatment or immunosuppressives for solid organ transplants.

Tinea versicolour infection produces hyper-or hypopigmented macules on the torso and proximal limbs with fine bran like scale. Infection can be chronic and recurrent with exacerbations following climatic changes in humidity. Organisms can be detected in a KOH preparation of skin scrapings. Treatment of pityriasis versicolour has traditionally been with selenium sulphide (Selsun® shampoo) applied as a cream to the affected areas twice daily or more recently with imidazole creams or foaming washes. Treatment needs to be applied to skin beyond the disappearance of the eruption, however, relapses are common with topical therapies. A course of oral ketoconazole or itraconazole for seven days is effective in eliminating the reservoir of Pityriasis organisms and helps prevent further relapses.

Tinea incognitaRefers to the specific clinical picture seen when a potent topical corticosteroid preparation is mistakenly applied to a tinea infection. Inflammatory features such as erythema may be absent; typically a mild, pink, scaly annular macule with central clearing is seen. Skin scrapings stained with KOH show abundant hyphae and permit the correct diagnosis.

Bacterial infections

ImpetigoA superficial bacterial infection characterized by honey-coloured crusts or vesicles on a moist erythematous base. Impetigo is highly infectious and is spread by direct contact or fomites and can infect intact skin. The organism(s) responsible are usually streptococcus or staphylococcus aureus. High ambient temperatures, humidity, low altitude and poor hygiene may favour development and transmission of impetigo. Streptococcal impetigo has spread amongst footballers and

those playing North American football. Treatment consists of topical or systemic antibiotics directed against both streptococcus and staphylococcus. Removal of crusts by gentle soaking with warm compresses of potassium permanganate (1 in 10 000) dilution followed by a topical antibiotic such as mupirocin or fusidic acid, for approximately seven to ten days is effective. The entire skin, scalp included, should be washed with an antiseptic soap daily for ten days. Alternatively, a ten day course of broad spectrum oral antibiotics active against ß-lactamase producing staphylococci is also efficacious.

The patient should be isolated until clearance of crusts and not allowed to compete in contact sports. In particular, sportsmen such as wrestlers should be free of new lesions for at least 48 hours prior to competition and should have no moist, exudative or draining lesions prior to tournament participation.

Pitted keratolysisA bacterial infection of the palmar surface of the feet due to superficial infection with corynebacterium species. It characteristically appears as shallow white pits or dents in the stratum corneum. Increased sweating (hyperhidrosis) is thought to play an aetiological role in the condition and thus may be seen with increased frequency in athletes. Maceration and malodour may be associated findings. Treatment consists of general preventative measures to control hyperhidrosis (absorbent socks, leather shoes, 'shoe-free' intervals), topical application of antiperspirants containing 20% aluminium chloride, an topical antibiotics such as 1-2% erythromycin or clindamycin solution.

Viral infections

Herpes simplex virus (HSV)HSV is a double stranded DNA virus which typically causes recurrent infections of the mucous an periorifical membranes. However, it can infect any skin surface and remain latent in the ganglia of peripheral nerves.

Herpes gladiatorumHerpes gladiatorum has been described in participants in close contact sports such as wrestling and rugby (also known in the latter as 'scrumpox') and in a recent study of American college wrestlers 7.6% were reported to have had a herpes skin infection in the preceding 12 months1. Herpes gladiatorum is transmitted primarily by direct skin to skin contact, and abrasions in the skin may allow a pathway of infection. The

majority of lesions occur on the head or face, followed by the trunk and/or extremities. A prodromal itching or burning sensation is followed by clustered vesicular lesions on an erythematous base which heal with crusts over about one to three weeks. Less commonly headache, malaise, sore throat and fever may accompany the primary infection. Recurrent episodes may occur following the initial infection and may precipitated by sunburn, illness, and emotional stress. HSV antibodies, acquired from previous cold sores, may be protective from acquiring herpes gladiatoraum eruptions. Because of its unexpected location on the cutaneous surface, herpes gladiatorum any be confused with impetigo, varicella, staphylococcal furunculosis, or allergic or irritant contact dermatitis. Adequate treatment, counseling and public health strategies depend on making an accurate diagnosis, hence viral immuno fluorescence and cultures should be obtained by gently breaking an intact vesicle and firmly rubbing the swab tip across the base of the erosion. Treatment of herpes gladiatorum is ideally with oral acyclovir (200mg five times a day for the five days) and is most effective if commenced at the first symptoms of an outbreak. Topical acyclovir is available but is probably less effective. Concomitant secondary impetiginisation should also be treated. HSV can survive for hours to days outside the host if environmental conditions are appropriate2 hence all contaminated surfaces should be cleaned with antiseptic solution. In the vesicular phase and until the crusts have separated, patients should avoid sports which could involve physical contact.

Molluscum contagiosumA highly infectious pox virus which can also be spread by human contact. The organism appears to be easily spread in an aqueous medium, for example, in communal baths, spas and pools. Amongst athletes, swimmers and cross country runners have the highest incidence of mollusca. Their incidence may be increased in patients with underlying active atopic dermatitis. They typically appear as solitary or multiple flesh-coloured dome shaped papules with a central umbilication. The differential diagnosis includes multiple basal cell carcinomata, cryptococcosis and appendageal tumours such as trichoepitheliomas. They can be treated by gently breaking the surface of the lesion and extracting the central keratinous plug. Other treatments employed are cryosurgery with liquid nitrogen, electrodessication and topical trichloroacetic acid or tretinoin. Athletes may resume contact sports 48 to 72 hours after the lesions have cleared.

Common wartsAre epidermal growths caused by infection by the human papillomavirus group (HPV). Infection can occur if infected debris from warts comes in contact with abraded skin and can result in either autoinoculation or transmission to susceptible individuals. However, it is not generally thought to be highly infective and thus not limit participation in contact sports. Plantar warts can cause pain with ambulation, thereby limiting performance in sporting activities. Warts may also be more common in callouses which develop in sport. Paring of plantar warts with a #15 blade reveals small black spots corresponding to thrombosed capillaries within papillae, thus distinguishing the lesions from callouses or corns, which lack these dots and have a central hyaline core. Treatment of plantar warts is challenging and may cause as much inconvenience to the athlete as the presence of the wart itself. Daily application of salicylic and lactic acid preparations under occlusion with concomitant paring with an emery board may be effective, as may repeated cryosurgery and paring at two or three week intervals. For resistant warts, intralesional bleomycin injections or carbon dioxide ablation can be used. Oral high dose Cimetidine therapy (30-40mg/kg/day) has reportedly been successful in childhood warts; however other studies have shown no advantage in Cimetidine over placebo in adults.


Introduction

Psychological principles of peak performance

Stress management

Clinical problems: psychological disorders

Substance use problems

Psychological aspects of injury rehabilitation

Overtraining/exercise addiction

Interpersonal problems

Introduction

Sport psychology is practiced by psychologists specializing in the domain of sport psychology and by sport scientists specializing in psychological aspects of sport and the athlete. It concerns itself with the maximization of sporting performance by developing the mental strength and addressing the general psychological well-being of athletes. Sports psychologists from both backgrounds, have most often worked with athletes on mental or psychological skills training, which deals with topics such as motivation, confidence, arousal control, concentration, mental rehearsal, and life skills; usually addressed through an educational approach. Additionally, psychologists have become involved in a range of clinical issues with athletes and interpersonal issues between members of a team or between coaches and athletes. Contemporary sport psychologists endeavour to follow a scientist-practitioner model, where applied intervention is grounded in theory and research. However, intuition and clinical experience are also drawn upon, especially when there is no documented theory of significant research findings to guide intervention.

From a psychological perspective, athletes are best considered first as the same as non-athletes. Athletes have the same amount of psychological problems as non-athletes, although they do tend to have certain problems (e.g. eating disorders) a little more than the general population, while a slightly lower rate of chronic mental health problems (e.g. schizophrenia). This chapter is written with adult athletes in mind. However, it must be recognized that young athletes have a number of differing and special needs. Coverage of issues in relation to child and adolescent athletes are addressed in a number of specialist texts in the area.

Sport physicians need to know about a number of psychological factors, including those related to peak athletic performance, and those that effect injury recovery or contribute to injury. They also need to be aware of common psychological problems that an athlete may experience, and be able to recognize the signs and symptoms of an actual mental disorder. It is useful for physicians consulting with athletes to know basic treatment processes for psychological problems in order to undertake initial intervention with athletes, and for physicians to have some understanding of the type of intervention strategies applied by psychologists. Whenever referring to a sport psychologist, it is important to check their qualifications and

inquire as to their background and experience. Aim to match the psychologist's training and area of expertise with the athlete's needs. There are a number of difficulties with the psychologist seeing the athlete separate from there sporting environment. The ideal mode of operation for a sport psychologists is for them to work as part of the sports' science team, interacting with physicians, coaches, trainers and other support staff.

Psychological Principles of Peak Performance

Athletes endeavour to consistently perform to their maximum. Psychological factors are important determinants of peak sporting performance. A state indicative of peak performance has been coined 'being in the flow'. Features of the 'flow' state include:

· Being composed, but alert and energized (not too relaxed but not over aroused). Thriving on pressures, wanting to be involved in the action and being proactive.· Feeling of 'knowing what have to do', and belief that it can be done. Being ' focused' on the tasks at hand (not affected by distractions, a loss of self-consciousness), and having extraordinary awareness (clarity and certainty).· Displaying spontaneous and automatic activity (merging of action and awareness). Having timing, space and rhythm.· Well prepared physically and mentally, with both aspects peaking in harmony.

Through attention to these mostly mental aspects, athletes can move toward the achievement of peak performance. Five psychological principles evident in the description of the flow state are activation, concentration, confidence, motivation, and preparation.

Activation

The optimal level of activation is the most fundamental prerequisite for peak performance, and excessive anxiety the most common pre-competition worry for athletes. The relationship between arousal (the physiological component of anxiety) and performance is best understood diagrammatically. (Fig. 1). Although other models (e.g. reversal theory) have become more popular, the inverted-U hypothesis portrayed in Fig. 1 remains the most applied model of arousal control. The

model indicates, that as arousal increases performance improves to a certain point, however, performance declines if arousal continues to climb. A curvilinear relationship exists between arousal and performance. Too much or too little arousal impairs performance. The desirable state (optimal arousal level) is at the point before the curve arches downwards or where the line levels off. This point (illustrated in Fig. 1) varies according to sporting task and across individuals. A variation on this model, the catastrophe theory, indicates that the arousal-performance relationship is not symmetrical. Instead, once anxiety exceeds appropriate levels performance deteriorates rapidly rather than gradually.

Treatment: If an athlete is experiencing too much anxiety, intervention at both somatic and cognitive levels should be conducted. Arousal can be lowered through relaxation exercises (e.g. deep diaphragmatic breathing, progressive muscle relaxation, biofeedback). Psychologists train athlete's in mental strategies to help control dysfunctional thoughts (which are essentially perceptions of environmental demands), effectively plan for sporting tasks, and build self-confidence. Behavioural interventions such as systematic desensitization (where through gradual exposure athletes come to tolerate situations that created anxiety or discomfort for them -see 'Anxiety Disorders') and performance simulation are also applied if appropriate. Additionally, coaches can be educated on how to lower the pressures on their athletes. In extreme cases, athletes may be experiencing symptoms of an anxiety disorder which require clinical attention (see later).It must not be neglected that athletes can also be under aroused, a state often associated with apathy and a lack of focus or wandering thoughts. As with over arousal, multimodial intervention needs to be conducted to 'Psych-up lethargic or unassertive athletes.

Concentration

Concentration, attention or focus is also a significant element of successful sporting performance. Athletes (as with humans generally) have limitations in what they can attend to at any one time. Athletes need to display selective attention or be 'focused on the right thing at the right time'. Athletes need to:

· Concentrate on task salient cues (events or things in the environment) while simultaneously ignoring extraneous or irrelevant information. This includes focusing on the present

and putting aside previous error of successes.· Display flexibility or shiftability in their concentration (i.e. alter width and direction of attention). This includes switching to relaxing cues after or in between intense mental efforts in order to regulate mental energy.· Sustain alertness (sensitivity to environment) throughout sporting events, and respond quickly to events.

A widely applied model of attentional focus is presented in Fig. 2. The dimension of direction refers to the source of things attended to; either in the sporting environment (external) or within the individual (internal). The dimension of width refers to the number of cues that receive attention at one time; ranging from broad (many cues) to narrow (a few cues only). Skilled athletes switch between cues that are optimally task-relevant (including refocusing after distraction). For example, they move attention from play in general (broad focus) to the particular motor skill they are performing (narrow focus). If athletes do not maintain the appropriate attentional style (i.e., broad-internal, narrow-internal, broad-internal, narrow-external) for the various tasks they perform (examples depicted on graph) they will have problems. Athletes can also be negatively affected by overloads of internal (e.g. to many instructions or game plans to apply) or external (e.g. lots of other competitors to watch) stimuli.

Treatment: For some athletes, a clear and practical description of the Nideffer model is sufficient for the self-development of positive attentional strategies. Other athletes, may require more intensive training in concentration. Generic and sport-related interventions include: exercises for clearing the mind (letting thoughts go), the maintenance of focus on a particular object/s, the performance of mental tasks while confronted with distractions, and cognitive structuring (e.g. parking thoughts); controlled breathing; goal setting/performance planning; positive self-talk; mental rehearsal; the development of cue words or checklists (events, things or thoughts for an athlete to associate with specific concentration points, e.g., 'head down' when shooting for goal); performance simulation; and the use of biofeedback and video feedback equipment. Regular practice of skills is essential if athletes are to improve. An individualized training program can be developed according to the assessment of attentional deficits (the TAIS questionnaire-based on the Nideffer model-can be used). Long-term or consistent deficits in an athlete's concentration may be due to, or symptomatic of, some psychopathological problem requiring

clinical attention.

Motivation

It is virtually essential for athletes to be motivated and confident. Motivation involves the energization and direction of behaviour. Individuals vary in the degree they are influenced by intrinsic/internal (e.g. fun, personal mastery) or extrinsic / external (e.g. approval from significant others, material rewards, winning) sources of motivation. Similarly, achievement orientation (an ego or task goal approach to performance, and desire for success or fear of failure) differs among athletes. Furthermore, as an athlete experiences transitions in their life, sources of motivation are likely to change in a corresponding manner.

Treatment: An understanding of what is important to each particular athlete, is a prerequisite for intervention to increase motivation. Also, any reasons for a loss in motivation should be assessed. Research has found that internal sources of motivation (because the involve factors which athletes' have control over) and a positive task orientation (which leads to greater intensity and persistence) are most related to successful performance. These factors, in conjunction with each individual athlete's identified sources of motivation, should be addressed in an enthusiastic manner with the athlete. It is useful to bring in a person who is held in high regard by the athlete and has good communication skills to discuss such issues with the athlete. As a protocol, it is important: to never assume what motivates each athlete, to not overestimate the importance of personality factors (traits) relative to environmental influences, and to have athletes focus on achieving positives rather than avoiding negatives. The setting of specific, challenging, but realistic goals is the most commonly used strategy to aid motivation.

Confidence

An athlete's self-confidence encompasses their general state of being and their confidence in undertaking specific sporting tasks of relevance. Self-confidence has a large cognitive element, whereby a person forms subjective judgements about their ability to successfully perform certain tasks or meet certain environmental demands. The point that perceptions and attitudes are involved forms the basis for interventions aimed at improving an athlete's self-confidence.

Treatment: Strategies that can be used (in conjunction with

coaches) to raise an athlete's confidence in relation to sporting tasks include: imagery of successful performance accomplishments, actual successful performance accomplishments (through favourable game simulations and drills at training), utilization of genuine and credible verbal reinforcement from coaches and peers, frequent self affirmations, self-talk and thought control during performance, and the setting and subsequent achievement of appropriate attainable goals. Since athletes perceptions of their actual performance can override gains from most confidence-building techniques (performance accomplishments provide the most potent information for judgements related to self-confidence), mental skills trainers should aim to use previous successful performance as the primary catalyst for efficacy of future performance.

If an athlete is experiencing a general loss of confidence throughout their life, a psychologist can employ global strategies or undertake personal development focusing on the 'whole' person. As a first step in this therapeutic process, athletes explore their self-image and personal belief systems, identify aspects which provide barriers for them or which they require healing on, and emphasis the productive attitudes they hold. Changing confidence at this level takes time. Unconstructive thought patterns (e.g. constant attribution's in external or 'uncontrollables' terms) are usually entrenched.

Preparation

Surprisingly, the obvious prerequisite for success, preparation or organization, is frequently given insufficient attention by athletes. Athletes often need reminding about the importance of physically looking after themselves, following appropriate pre-competition routines, and having game plans, etc.

Stress Management

Because of the amount of exercise athletes undertake, they are often regarded as not being stressed. However, athletes' engage in exercise to achieve a high performance level, which places immense pressure on them, and means that they do not always achieve the health benefits that come with non competitive physical activity. Both sport-related rigours and non-sporting pressures (relationships, shortage of time, developing a career outside of sport, financial concerns) lead to specific

performance problems ( e.g. excessive self-focus, 'choking') and a general proneness to stress. Furthermore, with numerous physical and psychological demands due to intense training and competition over the course of their careers, athletes are susceptible to injury, overtraining and burn-out. In cases of burn-out (characterized by exhaustion, negative responses to others, depressed mood, and being overwhelmed by stressors), time away from sport for re-assessment of goals and the undertaking of stress management is a necessity. Interventions in regard to injuries and overtraining are discussed in detail in later sections of this chapter.

Stress management intervention involves techniques employed in anxiety control for somatic and cognitive aspects (see 'Activation' subsection), training in planning and organizational skills, and coping strategies for dealing with pressure. A role of the sport psychologist is to facilitate the personal development of athletes; to assist them to develop, and effectively use, a range of coping strategies and problem solving processes. This includes removing maladaptive strategies an athlete has applied (e.g. excessive avoidance behaviour or withdrawal, substance use-see later section) and devising interventions that improve the ways he or she copes with sport-specific and life stressors. Assessment of the athlete's current coping strategies is an important part of the process of determining the most useful intervention mix. An athlete's coping style can be monitored through questionnaires such as the WOCS (Ways of Coping With Sport), and MAPS (Mental Attributes of Performance). Response patterns can be considered in relation to sport-specific research on the most effective or adaptive coping styles. A model for training coping skills involves instruction in the control of emotions, organizing and filtering feedback information, planning responses, and executing responses. It should be particularly noted, that in team sports, each individual athlete has additional resources to draw upon (teammates), but also additional stressors.

Individual differences

It is of interest to know, that the existence of intuitively appealing relationships between sport and personality can be accorded only mythological status. Research has failed to show either that success in sport depends on the possession of certain personal characteristics, or that certain individuals are best suited to certain sports or positions.Although personality traits offer little discrimination between athletes, or between athletes and non athletes, there are some

individual differences (ID's) in sport to consider:

1) There are ID's on the dimensions of anxiety, concentration and mood. These vary according to sporting tasks and /or whether athletes are skilled or novice performers. Psychometric tests such as the SCAT (Sport Competition Anxiety Test - and the later version, CSAI-2), the TAIS (Test of Attentional and Interpersonal Style), and the POMS (Profile of Mood Sates) measure athletes level of anxiety, style of attention, and mental strength respectively. Athletes with inappropriate scores on these factors can benefit from the interventions outline in the previous sections of this chapter.

2) There are ID's in the prevalence of certain mental disorders across sports. Suggestions that a higher prevalence of personality disorders exists among martial arts participants has antidotal support, while there is epidemiological data to validate the assumed higher prevalence of eating disorders among gymnasts


Introduction

Principles of rehabilitation

Key concepts

Treatment modalities

Rehabilitation of four common injuries.

Complications of rehabilitation

Prevention

'Life is movement, movement is life'. Aristotle

Introduction

Rehabilitation is a generic term for the comprehensive treatment of injury and/or medical conditions. It has active and passive elements. It focuses upon the whole person not just the

injury and aims to restore the greatest possible degree of function in the shortest possible time. The factors implicated in the cause of injury should be addressed to prevent injury recurrence. Three concepts help with the understanding of the rehabilitation process these are impairment, disability and handicap.

Injury causes an individual an impairment. This is the injury at the tissue level e.g. ruptured medial collateral ligament of the knee.Impairment usually causes a disability This is a loss of function e.g. walking with a limp and unable to run. This in turn may cause a handicap this is an individuals inability to perform tasks or engage in activities. e.g. the professional footballer is unable to compete for the rest of the season due to the knee injury which causes loss of playing time, reducing his income and prematurely ending his career. This causes some reactive depression.From this example the need for the physician to consider the medical, physical, psycho-social, vocational and leisure requirements of the injured athlete is apparent.

The areas covered are1. the principles of rehabilitation.2. treatment modalities3. specific examples4. complications of inadequate or incorrect rehabilitation5. prevention

Principles of rehabilitation

The process of athletic injury rehabilitation aims to minimize tissue damage and allow a safe return to activity. It is based on the science of tissue healing, knowledge of joint biomechanics, physiology of muscular strength and endurance, and the neurophysiological basis of skill retraining. Successful programs are based on an understanding of these constraints, which, when properly applied, permit the progressive activity of joints and muscles. Muscular strength, endurance and power are redeveloped while flexibility and cardiovascular fitness are maintained. Precipitating factors are identified and addressed to minimize reinjury.

To understand, grade and treat injuries the physician needs to identify the tissues involved. This chapter focuses on muscle-

skeletal injury and rehabilitation of bone, ligament, muscle, tendon, connective tissue and neuromuscular structures combining to produce coordinated, purposeful movement. The treatment of other injuries is covered in relevant chapters.

The healing process involves inflammatory, repair and remodeling phases. There are detrimental effects of immobilization, muscle wasting and weakness and subsequent joint damage. This leads to further immobilization and reflex inhibition 'a vicious circle'. Early mobilization is usually indicated. Lack of motion of joints results in shortening of capsular and other connective tissue structures supporting the joint, loss of lubrication and alternating compression between joint surfaces deprives articular cartilage of nutrition. There are detrimental systemic effects of immobilization, these begin within hours and become clinically important within days. They include cardiovascular deconditioning, nervous system depression, skin sores, gastrointestinal complaints (constipation), thromboembolic genesis, bone resorbtion and respiratory impairment. Thus the expression 'MOVE IT OR LOSE IT'

An understanding of the sport or activity is required, many injuries are sport specific and communication is enhanced if the physician has some basic knowledge of the sports requirements. 'Profiling' is a concept that matches an individuals physiognomy with the type of athletic activity and in team sports their role.

Key concepts

Team Approach

Rehabilitation is facilitated by a team approach. The basic team comprises in order of importance

· The injured athlete.· The physical therapist- physiotherapist have the most scientific training (other types include masseuse)· The doctor.· Others; orthotist, brace maker, strapper, coach, exercise trainers, dietitian, psychologist, dentist, nurse, first aid personal, peer group, family and friends.

Diagnosis

Historypresent injury, past, athletic, social, family and psychological histories where requiredExaminationincluding measurement of impairment and function, comparison with unaffected limb and review of biomechanical factors.Investigationsthis may include specific functional tests, pathology, radiology and nuclear medicine investigations where appropriateProblem listparticularly if the injury is complex or severe.

Acute injury management (Table 1)

Begins immediately and can be performed by the athlete or any other capable person. This phase lasts the first 24-48 hours. It consists of protecting the individual from further harm, resting, and icing the injury. Compression and elevation are used to minimize edema and haemorrhage and drugs are used for analgesia, anti-inflammatory properties and muscle spasm relief. Acute injury management is summarized by the acronym P R I C E. Occasionally more extensive treatment or surgery is required.

Drugs

In general the authors feel that drug use should be minimized and the other components of injury management emphasized. Drugs used in rehabilitation of sports injuries are of four main groups.

1. Analgesics - paracetamol, codeine, opiates and local anesthetic agents.

2. Anti- inflammatory medications are used extensively and have analgesic properties as well as causing moderation of the inflammatory response to injury. A short course of 3-7 days can be useful. Compliance is better with once or twice daily dosing. Topical and parental antiinflammatory medications are now available. Gastric ulceration, hypertension and renal impairment are among the side effects.

3. Anti spasmodics and sedatives are utilized to reduce muscle spasm and consequent pain, stiffness and immobility in the first 48 hours. They also induce drowsiness and can aid sleep. Benzodiazepams are used with caution as they affect balance,

coordination and judgment.

4. Corticosteriods are usually used in chronic injuries. They have anti inflammatory, immunological and metabolic effects. They are injected intra-articularly or into connective tissue around tendons e.g. in subacromial bursitis. Their efficacy has been established. There are severe potential complications such as septic arthritis and tendon rupture these agents should be used by experienced practitioners only. Do not use on the Achilles tendon.

Treatment modalities

Passive physical treatments

(used alone or in combination)

Ice Heat Ultrasound T.E.N.S. Laser Manual Therapy

Ice has beneficial effects in the acute and intermediate phases(8). Cold decreases spasm and slows nociceptor nerve conduction. Once swelling and pain have diminished sufficiently, ice is combined with active and passive range of motion within pain tolerance. The ice is used both prior to and during the therapeutic exercise session. This is done for 20-30 minutes twice a day. In between the injury site is protected. Induce analgesia with ice for 20 minutes, exercise (static stretch, isometric contract, static stretch), rest 30 seconds and repeat (2-3 times) several times per day. Once the effects of swelling and pain have subsided and the athlete has progressed to more vigorous exercise and functional activity, the ice is used for 20-30 minutes after the therapeutic exercise bout. Note: Ice can cause burns and superficial nerve palsies (peroneal and ulnar) Ice pack; Plastic bag, crushed ice, tea towel. Caution should be exercised with Gel packs which freeze below 0 Centigrade. These should be wrapped in toweling.

Heat causes vasodilatation (increased delivery oxygen, nutrients and immune mediators) and increased metabolic rate, altered pain sensation, increased collagen extensibility, better nutrition and decreased sensitivity to muscle stretch(9). Acute

use helps relieve muscle spasm. Most useful for chronic inflammation, joint stiffness, pain syndromes. Note: May cause increased edema and local burns and should be supervised by the physical therapist.

Modern use of heat relies on hot packs 40-70 degrees applied for 20 minutes in conjunction with range of motion exercises. The widespread use of rubifactents to cause peripheral vasodilatation and local heating is not recommended due to the relative difficulty in controlling timing and dosage.

Ultrasound. High frequency soundwaves 0.8- 1.1MHz, produce heating at fascial planes. When pulsed at low frequency ultra sound produces a mechanical effect. Together they produce an analgesic and anti-inflammatory effect by increasing local perfusion and metabolism.Thrombolysis is aided and there is a role in haematoma treatment. There are complications of overzealous or incorrect treatment. Usually employed after the acute phase.

TENS transcutaneous electric nerve stimulation produces analgesia and is used extensively in chronic pain syndromes. Works via spinal gate mechanism and direct effects on nociceptors. Indifferentual is a form of TENS in which alternating electrical stimulation is used to produce various levels of muscle contraction. This reduces the edema and helps minimize disuse atrophy. There is some evidence that it has antispasmodic action in spinal injury patients.

Laser. Cold laser is used for small localized lesions (e.g. long head biceps strain) It is claimed to reduce pain and spasm and have beneficial effects on local metabolism. Evidence exists for alteration of nerve conduction but is absent for clinical effect in well controlled in vivo studies.

Manual therapy. This differs from the above modalities in that it requires the therapists to use their bodies on the patient. Manual therapy encompasses all forms of massage, mobilization, manipulation, traction and neural stretching. The ultimate manual treatment consists of surgery. The individual techniques and combinations applied vary and are beyond the scope of this chapter. Manual therapy is the most ancient form of medicine the 'laying on of hands' Several practitioner groups make claims that are unscientific and misleading. The authors recommend that athletes be guided to therapists who have scientific training, experience in sports injury and who can work in a team. There are potential risks with manual

therapy, particularly rotational spinal manipulation which has caused disc prolapse, corda equina lesions and vertebral artery dissection. There are clear benefits in reduction in muscle spasm and edema, relaxation, flexibility and increased joint range of motion from manual therapy. There is also a placebo effect in some patients. Psychological benefits of manual therapy are often observed.

Active physical treatments

Active physical treatment is the foundation of the rehabilitation process. When an injury occurs immobile muscle rapidly atrophies, connective tissue contracts and detrimental joint changes occur. Active physical treatment requires the interest and compliance of the athlete to minimize injury consequences and return to activity.

Strengthening exercises (Fig 1-14).These aim initially to minimize disuse atrophy, increase circulation and maintain muscle condition. As healing continues gains in strength, control, co-ordination and endurance facilitate recovery. There are several types of strengthening exercises and these are combined for maximum effect.

Isometric exercises are conducted without movement across the joint on which the muscle acts. There are two program types prolonged contraction involves a 20 - 30 second contraction performed 10 -20 times with a 20 second break. These can be performed from the acute phase of injury up to 10 times per day. Basmajian recommends brief (5-6 sec) repeated isometric maximal (added weight) exercises with a 20 sec delay. This minimizes cardiovascular stress (hypertension) which has been observed with prolonged isometric exercise. Isometric exercise can be performed with the joints in various angles and achieve improved strength of muscle.

Isotonic. In which muscle contraction moves a joint through a range of motion. Thus if the muscle shortens while contracting (e.g. biceps curl) it is termed a concentric contraction. The act of lowering a weight from height (e.g. lowering a biceps curl back to the start position) is termed eccentric as the muscle is lengthening while contracting. Daily progressive resistance exercise (P.R.E.) using weights or other resistant devices is prescribed and begins after the acute phase. Multiple repetitions are used and the number and resistance can be varied. The tempo or rest periods can also be progressively altered. Careful

instruction and supervision is required. Typical examples are provided later. A variety of machines have been designed to improve strengthening throughout the joint range for different muscle lengths. One type is a command system with increased weight at mid range and reducing at full extension and flexion (Nautilis)

Various machines have been developed to perform isokinetic exercise.This allows constant velocity with variable resistance as the muscle move the joint through its range. An example is the isokinetic dynamometer machine which was originally designed for rehabilitation of knee injuries. It can be applied to any joint.

Balance around a joint is essential in any exercise program with a balanced ratio of agonist and antagonist training. Coordinated patterns of training are covered in functional training.

Plyometric exercises are also useful in developing muscle power .They use a stretch-shortening cycle to elicit a more forceful concentric contraction. Associated with rapidly changing eccentric to concentric action, it has been suggested that they may develop reciprocal reflex training which may be useful in injury prevention. It is used 2-3 times per week but discontinued if the athlete develops pain, swelling or other signs of overuse. It has also been employed as a strengthening technique in uninjured athletes.

FlexibilityFlexibility exercises have two benefits. First in allowing and encouraging joint ROM exercises, they are a factor in return of normal joint mechanics. Second the effect of graduated stretching over time increases the length of contractile units and connective tissue elements within the muscle. As the muscle, tendon and enthesis are part of the same contractile unit this helps reduce injury. Blood supply to the tendon is predominately from the muscle with less from the bone attachment/enthesis. There is a critical area in the tendon which is susceptible to injury and ischaemia.

Flexibility exercises have the effect of improving the efficient range of muscle contraction and preventing avulsion at tendon bone junction by reducing the chance of end range 'bow stringing'. After injury stretching after physical therapy such as

ice or heat reduces the activity of the fusimotor system, provides analgesia and often allows a greater ROM.

Stretching regimes are from 30~60 seconds; times 3 repetitions; twice daily. Ballistic (bouncing) exercises or passive stretches by weights machines or trainer, run the risk of muscle tears. A slow stretch and creep technique is preferred, progressive to the limit of discomfort and NOT beyond. The desired muscle length may require twice daily stretching for six weeks with maintenance once daily. Specific stretching exercise programs are available in many forms. A basic lower limb stretching is provided(Fig 15).

Proprioceptive Neuromuscular Facilitation Stretching (PNF) reduces muscle tone by stimulating the Golgi tendon organs. It relies on synergies using agonists activities to relax antagonists. PNF involves Proprioceptive and tactile techniques to cause muscle relaxation and repetitive activities to establish patterns of muscle contraction . Various movement and flexibility paradigms are prompted by diverse groups. These include yoga, Bowen and Alexander techniques and Feldenkrais. The authors believe that each has its merits although blindly following the teachings of self promoting 'gurus' is unscientific.

Endurance Endurance refers to the ability of a muscle to perform a static (isometric) or dynamic (isotonic) task. It depends on the state of the individual muscle and the cardiovascular status of the individual.

A guide to endurance can be made by using physical work capacity measures, or pulse verses workload. A linear relationship exists between oxygen uptake and pulse rate. Using the Astrand nomogram a predicted VO2 maximum may be determined (26).Other protocols have been used in cardiovascular testing. An example is the step test whereby the number of steps of a given height from the floor, up to a bench, taken in a given period is recorded.

As a minimum cardiovascular and endurance training should occur 20 minutes, 3 times weekly . Most athletes will easily exceed these guidelines. For an in depth description of cardiovascular fitness and aerobic exercise readers are referred

to exercise physiology texts. The benefits include cardiovascular training, metabolic stimulation, maintenance of muscle bulk release of endocrine hormones and immunological modulation. There is evidence that endurance training of unaffected body parts has trophic effects on the injured area. It also may have positive psychological effects in individuals (27).

Many methods are available to provide aerobic and endurance training for the injured athlete.

They include:· Swimming· Water exercises(hydrotherapy)· Brisk walking· Circuit training· Calisthenics/ Aerobics· Stationary bicycles· Machines (stepper, rowing, arm crank etc)

Swimming is the preferred exercise in most cases as the activity is non weight bearing and is less prone to re injury. The particular regime will depend on the site, nature and age of injury and on the individuals circumstances and skills.

Proprioceptive retrainingLigaments and to some extent tendon injuries are accompanied by an impairment of proprioception which may persist after the inflammatory phase of the injury is resolved. The three cues to balance are vision, vestibular function and lower limb position sense - proprioception.

Following an injury, position sense of a body part in relation to space or other objects is often diminished or lost. The goal of proprioceptive exercises is to reduce the time between neural stimuli and muscular response, thus reducing the stress on the injured joint during functional activities. Rehabilitation of injuries to the knee and ankle require proprioceptive retraining. Whiplash injuries cause abnormal neck proprioception and upper limb injuries may also require retraining.

The components of lower limb proprioceptive training include:

· Taping or external supports to provide increased sensory input and protection during the early phases.· Static balance exercises standing on one leg initially then

graduating to less firm surfaces e.g. foam and eventually wobble board.· Reduction of visual cues using blindfold or distracting activities during balance exercises e.g. throwing a ball to and from trainer or against a wall and catching. · Dynamic training such as jogging in soft sand progressing to figure of eight or zig zag patterns. During the later stages of recovery jogging on firm surfaces then finally uneven surfaces

Functional training Functional training begins as the healing process allows. It is composed of the components already mentioned. Strength, flexibility, propioception and endurance are required.

Muscle groups are exercised in tandem allowing coordinated purposeful movement. Specific weakness patterns and technique errors can be addressed. This then has benefits on strength and endurance allowing further functional training. These exercises may begin with partial squats, leg presses, step-ups, lunges, or closed-chain terminal knee extension. As symptoms subside and function improves devises such as reciprocal (vertical or stair) climbers, lateral slide boards, treadmills are used. A progressive walk-jog-run program can begin as healing proceeds. For Example, a basketball player with a knee injury could perform a compound exercise such as a set of body weight squats, when pain free. This could progress with increased weights and gradual introduction of standing jumping exercises. This could be enhanced with a plyometric program of exercises.

Functional Training can be general or sports specific. It can be supervised by trainers, therapists, coaches or parents. Athletes enjoy it and it is part of a graduated return to full activity. It is useful for acute and chronic injuries. It has been shown to decrease time off employment and speed return to sport.

Psychological

The athlete with an injury requires consideration, understanding and empathy. They may be suffering not only an injury but financial and emotional stress. Body image is very important to athletes as well as the endorphin drive they have to exercise. Research suggests that athletes respond to injury with mood disturbance and lowered self-esteem. Calm explanation of the diagnosis, education and involvement in the rehabilitation plan are important parts of the therapeutic relationship. More time is

often required than with other patients but the usual excellent results offer the clinician satisfaction.The recruitment of the athlete to taking an active role in their rehabilitation will facilitate the process.In extreme cases a reactive depression or post traumatic stress may intervene. These may be treated by supportive psychotherapy and appropriate medication. Following physical recovery confidence and athletic performance may be slower to return. Education ,explanation and support are required. A Sports Psychologist may help.

Biomechanical factors

Understanding the mechanism of the injury will help modify the activity to prevent reinjury. If this is not corrected adaptive protective behavior may lead to a second and apparently unrelated injury. Biomechanical factors can be assessed by attending the events and being involved as team doctor. A detailed history and examination of the athlete is essential. Some sports have inherent physical demands which cause particular injuries e.g. female gymnastics forces girls to hyper-extend their backs and weight bear on the upper limbs leading to injury rates approaching 30% per year!.

Some injuries are caused by combinations of athletic activity, technique and individual anatomy. Plantar fascitis in which biomechanical factors are crucial in the prevention, treatment and rehabilitation is a good example.Subtle abnormalities at a high level of skill may only be diagnosed by video, gait and force plate analysis. A coach may help in these areas for technique advice. Foot wear modifications may be the logical starting point for runners. e.g. ilio tibial band friction syndrome may be improved by reducing tibial rotation by insertion of an anti-pronation shoe or orthoses.

Return to sport (Table2)

When the components of the rehabilitation process have been applied correctly the synergist nature of the treatment should enable return to sport. After a subjective assessment from the therapist or trainer that the athlete is able to use the injured extremity well. The athlete's ability to demonstrate enough self-confidence to fully participate in these activities without experiencing pain, swelling or giving way is assessed.

The athlete progresses to sports-specific activities in a noncompetitive environment. Their performance should be critically evaluated by the rehabilitation team. Specific stress testing may be performed. (Table 2.)

Table 2 Guidelines for return to sport after injury

- Acute signs and symptomss have passed- Full functional use of all joints, adequate strength, and - proprioception to perform normal tasks- Normal mechanics of movement- Succesful performance of sport-specific activities at or above pre-injury level should be documented

Handbook of Sports Medicine

Documents

Transcript of Handbook of Sports Medicine